essay on cancer and its types

Essay on Cancer for Students and Children

500+ words essay on cancer.

Cancer might just be one of the most feared and dreaded diseases. Globally, cancer is responsible for the death of nearly 9.5 million people in 2018. It is the second leading cause of death as per the world health organization. As per studies, in India, we see 1300 deaths due to cancer every day. These statistics are truly astonishing and scary. In the recent few decades, the number of cancer has been increasingly on the rise. So let us take a look at the meaning, causes, and types of cancer in this essay on cancer.

Cancer comes in many forms and types. Cancer is the collective name given to the disease where certain cells of the person’s body start dividing continuously, refusing to stop. These extra cells form when none are needed and they spread into the surrounding tissues and can even form malignant tumors. Cells may break away from such tumors and go and form tumors in other places of the patient’s body.

Types of Cancers

As we know, cancer can actually affect any part or organ of the human body. We all have come across various types of cancer – lung, blood, pancreas, stomach, skin, and so many others. Biologically, however, cancer can be divided into five types specifically – carcinoma, sarcoma, melanoma, lymphoma, leukemia.

Among these, carcinomas are the most diagnosed type. These cancers originate in organs or glands such as lungs, stomach, pancreas, breast, etc. Leukemia is the cancer of the blood, and this does not form any tumors. Sarcomas start in the muscles, bones, tissues or other connective tissues of the body. Lymphomas are the cancer of the white blood cells, i.e. the lymphocytes. And finally, melanoma is when cancer arises in the pigment of the skin.

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Causes of Cancer

In most cases, we can never attribute the cause of any cancer to one single factor. The main thing that causes cancer is a substance we know as carcinogens. But how these develop or enters a person’s body will depend on many factors. We can divide the main factors into the following types – biological factors, physical factors, and lifestyle-related factors.

Biological factors involve internal factors such as age, gender, genes, hereditary factors, blood type, skin type, etc. Physical factors refer to environmental exposure of any king to say X-rays, gamma rays, etc. Ad finally lifestyle-related factors refer to substances that introduced carcinogens into our body. These include tobacco, UV radiation, alcohol. smoke, etc. Next, in this essay on cancer lets learn about how we can treat cancer.

Treatment of Cancer

Early diagnosis and immediate medical care in cancer are of utmost importance. When diagnosed in the early stages, then the treatment becomes easier and has more chances of success. The three most common treatment plans are either surgery, radiation therapy or chemotherapy.

If there is a benign tumor, then surgery is performed to remove the mass from the body, hence removing cancer from the body. In radiation therapy, we use radiation (rays) to specially target and kill the cancer cells. Chemotherapy is similar, where we inject the patient with drugs that target and kill the cancer cells. All treatment plans, however, have various side-effects. And aftercare is one of the most important aspects of cancer treatment.

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What Is Cancer?

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Breast cancer cell dividing, as seen using microscope.

A dividing breast cancer cell.

The Definition of Cancer

Cancer is a disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body.

Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and multiply (through a process called cell division) to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.

Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldn’t. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous ( benign ).

Cancerous tumors spread into, or invade, nearby tissues and can travel to distant places in the body to form new tumors (a process called metastasis ). Cancerous tumors may also be called malignant tumors. Many cancers form solid tumors, but cancers of the blood, such as leukemias , generally do not.

Benign tumors do not spread into, or invade, nearby tissues. When removed, benign tumors usually don’t grow back, whereas cancerous tumors sometimes do. Benign tumors can sometimes be quite large, however. Some can cause serious symptoms or be life threatening, such as benign tumors in the brain.

Differences between Cancer Cells and Normal Cells

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Cancer cells differ from normal cells in many ways. For instance, cancer cells:

grow in the absence of signals telling them to grow. Normal cells only grow when they receive such signals.
ignore signals that normally tell cells to stop dividing or to die (a process known as programmed cell death , or apoptosis ).
invade into nearby areas and spread to other areas of the body. Normal cells stop growing when they encounter other cells, and most normal cells do not move around the body.
tell blood vessels to grow toward tumors. These blood vessels supply tumors with oxygen and nutrients and remove waste products from tumors.
hide from the immune system . The immune system normally eliminates damaged or abnormal cells.
trick the immune system into helping cancer cells stay alive and grow. For instance, some cancer cells convince immune cells to protect the tumor instead of attacking it.
accumulate multiple changes in their chromosomes , such as duplications and deletions of chromosome parts. Some cancer cells have double the normal number of chromosomes.
rely on different kinds of nutrients than normal cells. In addition, some cancer cells make energy from nutrients in a different way than most normal cells. This lets cancer cells grow more quickly.

Many times, cancer cells rely so heavily on these abnormal behaviors that they can’t survive without them. Researchers have taken advantage of this fact, developing therapies that target the abnormal features of cancer cells. For example, some cancer therapies prevent blood vessels from growing toward tumors , essentially starving the tumor of needed nutrients.

How Does Cancer Develop?

Cancer is caused by certain changes to genes, the basic physical units of inheritance. Genes are arranged in long strands of tightly packed DNA called chromosomes.

Cancer is a genetic disease—that is, it is caused by changes to genes that control the way our cells function, especially how they grow and divide.

Genetic changes that cause cancer can happen because:

of errors that occur as cells divide.
of damage to DNA caused by harmful substances in the environment, such as the chemicals in tobacco smoke and ultraviolet rays from the sun. (Our Cancer Causes and Prevention section has more information.)
they were inherited from our parents.

The body normally eliminates cells with damaged DNA before they turn cancerous. But the body’s ability to do so goes down as we age. This is part of the reason why there is a higher risk of cancer later in life.

Each person’s cancer has a unique combination of genetic changes. As the cancer continues to grow, additional changes will occur. Even within the same tumor, different cells may have different genetic changes.

Fundamentals of Cancer

Cancer is a disease caused when cells divide uncontrollably and spread into surrounding tissues.

Cancer is caused by changes to DNA. Most cancer-causing DNA changes occur in sections of DNA called genes. These changes are also called genetic changes.

A DNA change can cause genes involved in normal cell growth to become oncogenes. Unlike normal genes, oncogenes cannot be turned off, so they cause uncontrolled cell growth.

In normal cells, tumor suppressor genes prevent cancer by slowing or stopping cell growth. DNA changes that inactivate tumor suppressor genes can lead to uncontrolled cell growth and cancer.

Within a tumor, cancer cells are surrounded by a variety of immune cells, fibroblasts, molecules, and blood vessels—what’s known as the tumor microenvironment. Cancer cells can change the microenvironment, which in turn can affect how cancer grows and spreads.

Immune system cells can detect and attack cancer cells. But some cancer cells can avoid detection or thwart an attack. Some cancer treatments can help the immune system better detect and kill cancer cells.

Each person’s cancer has a unique combination of genetic changes. Specific genetic changes may make a person’s cancer more or less likely to respond to certain treatments.

Genetic changes that cause cancer can be inherited or arise from certain environmental exposures. Genetic changes can also happen because of errors that occur as cells divide.

Most often, cancer-causing genetic changes accumulate slowly as a person ages, leading to a higher risk of cancer later in life.

Cancer cells can break away from the original tumor and travel through the blood or lymph system to distant locations in the body, where they exit the vessels to form additional tumors. This is called metastasis.

Types of Genes that Cause Cancer

The genetic changes that contribute to cancer tend to affect three main types of genes— proto-oncogenes , tumor suppressor genes , and DNA repair genes. These changes are sometimes called “drivers” of cancer.

Proto-oncogenes are involved in normal cell growth and division. However, when these genes are altered in certain ways or are more active than normal, they may become cancer-causing genes (or oncogenes), allowing cells to grow and survive when they should not.

Tumor suppressor genes are also involved in controlling cell growth and division. Cells with certain alterations in tumor suppressor genes may divide in an uncontrolled manner.

DNA repair genes are involved in fixing damaged DNA. Cells with mutations in these genes tend to develop additional mutations in other genes and changes in their chromosomes, such as duplications and deletions of chromosome parts. Together, these mutations may cause the cells to become cancerous.

As scientists have learned more about the molecular changes that lead to cancer, they have found that certain mutations commonly occur in many types of cancer. Now there are many cancer treatments available that target gene mutations found in cancer . A few of these treatments can be used by anyone with a cancer that has the targeted mutation, no matter where the cancer started growing .

When Cancer Spreads

Drawing that shows metastasis, when a primary cancer spreads from its first location to other parts of the body.

In metastasis, cancer cells break away from where they first formed and form new tumors in other parts of the body.

A cancer that has spread from the place where it first formed to another place in the body is called metastatic cancer. The process by which cancer cells spread to other parts of the body is called metastasis.

Metastatic cancer has the same name and the same type of cancer cells as the original, or primary, cancer. For example, breast cancer that forms a metastatic tumor in the lung is metastatic breast cancer, not lung cancer.

Under a microscope, metastatic cancer cells generally look the same as cells of the original cancer. Moreover, metastatic cancer cells and cells of the original cancer usually have some molecular features in common, such as the presence of specific chromosome changes.

In some cases, treatment may help prolong the lives of people with metastatic cancer. In other cases, the primary goal of treatment for metastatic cancer is to control the growth of the cancer or to relieve symptoms it is causing. Metastatic tumors can cause severe damage to how the body functions, and most people who die of cancer die of metastatic disease.

Tissue Changes that Are Not Cancer

Not every change in the body’s tissues is cancer. Some tissue changes may develop into cancer if they are not treated, however. Here are some examples of tissue changes that are not cancer but, in some cases, are monitored because they could become cancer:

Hyperplasia occurs when cells within a tissue multiply faster than normal and extra cells build up. However, the cells and the way the tissue is organized still look normal under a microscope. Hyperplasia can be caused by several factors or conditions, including chronic irritation.
Dysplasia is a more advanced condition than hyperplasia. In dysplasia, there is also a buildup of extra cells. But the cells look abnormal and there are changes in how the tissue is organized. In general, the more abnormal the cells and tissue look, the greater the chance that cancer will form. Some types of dysplasia may need to be monitored or treated, but others do not. An example of dysplasia is an abnormal mole (called a dysplastic nevus ) that forms on the skin. A dysplastic nevus can turn into melanoma, although most do not.
Carcinoma in situ is an even more advanced condition. Although it is sometimes called stage 0 cancer, it is not cancer because the abnormal cells do not invade nearby tissue the way that cancer cells do. But because some carcinomas in situ may become cancer, they are usually treated.

Normal cells may become cancer cells. Before cancer cells form in tissues of the body, the cells go through abnormal changes called hyperplasia and dysplasia. In hyperplasia, there is an increase in the number of cells in an organ or tissue that appear normal under a microscope. In dysplasia, the cells look abnormal under a microscope but are not cancer. Hyperplasia and dysplasia may or may not become cancer.

Types of Cancer

There are more than 100 types of cancer. Types of cancer are usually named for the organs or tissues where the cancers form. For example, lung cancer starts in the lung, and brain cancer starts in the brain. Cancers also may be described by the type of cell that formed them, such as an epithelial cell or a squamous cell .

You can search NCI’s website for information on specific types of cancer based on the cancer’s location in the body or by using our A to Z List of Cancers . We also have information on childhood cancers and cancers in adolescents and young adults .

Here are some categories of cancers that begin in specific types of cells:

Carcinomas are the most common type of cancer. They are formed by epithelial cells, which are the cells that cover the inside and outside surfaces of the body. There are many types of epithelial cells, which often have a column-like shape when viewed under a microscope.

Carcinomas that begin in different epithelial cell types have specific names:

Adenocarcinoma is a cancer that forms in epithelial cells that produce fluids or mucus. Tissues with this type of epithelial cell are sometimes called glandular tissues. Most cancers of the breast, colon, and prostate are adenocarcinomas.

Basal cell carcinoma is a cancer that begins in the lower or basal (base) layer of the epidermis, which is a person’s outer layer of skin.

Squamous cell carcinoma is a cancer that forms in squamous cells, which are epithelial cells that lie just beneath the outer surface of the skin. Squamous cells also line many other organs, including the stomach, intestines, lungs, bladder, and kidneys. Squamous cells look flat, like fish scales, when viewed under a microscope. Squamous cell carcinomas are sometimes called epidermoid carcinomas.

Transitional cell carcinoma is a cancer that forms in a type of epithelial tissue called transitional epithelium, or urothelium. This tissue, which is made up of many layers of epithelial cells that can get bigger and smaller, is found in the linings of the bladder, ureters, and part of the kidneys (renal pelvis), and a few other organs. Some cancers of the bladder, ureters, and kidneys are transitional cell carcinomas.

Soft tissue sarcoma forms in soft tissues of the body, including muscle, tendons, fat, blood vessels, lymph vessels, nerves, and tissue around joints.

Sarcomas are cancers that form in bone and soft tissues, including muscle, fat, blood vessels, lymph vessels , and fibrous tissue (such as tendons and ligaments).

Osteosarcoma is the most common cancer of bone. The most common types of soft tissue sarcoma are leiomyosarcoma , Kaposi sarcoma , malignant fibrous histiocytoma , liposarcoma , and dermatofibrosarcoma protuberans .

Our page on soft tissue sarcoma has more information.

Cancers that begin in the blood-forming tissue of the bone marrow are called leukemias. These cancers do not form solid tumors. Instead, large numbers of abnormal white blood cells (leukemia cells and leukemic blast cells) build up in the blood and bone marrow, crowding out normal blood cells. The low level of normal blood cells can make it harder for the body to get oxygen to its tissues, control bleeding, or fight infections.

There are four common types of leukemia, which are grouped based on how quickly the disease gets worse (acute or chronic) and on the type of blood cell the cancer starts in (lymphoblastic or myeloid). Acute forms of leukemia grow quickly and chronic forms grow more slowly.

Our page on leukemia has more information.

Lymphoma is cancer that begins in lymphocytes (T cells or B cells). These are disease-fighting white blood cells that are part of the immune system. In lymphoma, abnormal lymphocytes build up in lymph nodes and lymph vessels, as well as in other organs of the body.

There are two main types of lymphoma:

Hodgkin lymphoma – People with this disease have abnormal lymphocytes that are called Reed-Sternberg cells. These cells usually form from B cells.

Non-Hodgkin lymphoma – This is a large group of cancers that start in lymphocytes. The cancers can grow quickly or slowly and can form from B cells or T cells.

Our page on lymphoma has more information.

Multiple Myeloma

Multiple myeloma is cancer that begins in plasma cells , another type of immune cell. The abnormal plasma cells, called myeloma cells, build up in the bone marrow and form tumors in bones all through the body. Multiple myeloma is also called plasma cell myeloma and Kahler disease.

Our page on multiple myeloma and other plasma cell neoplasms has more information.

Melanoma is cancer that begins in cells that become melanocytes, which are specialized cells that make melanin (the pigment that gives skin its color). Most melanomas form on the skin, but melanomas can also form in other pigmented tissues, such as the eye.

Our pages on skin cancer and intraocular melanoma have more information.

Brain and Spinal Cord Tumors

There are different types of brain and spinal cord tumors. These tumors are named based on the type of cell in which they formed and where the tumor first formed in the central nervous system. For example, an astrocytic tumor begins in star-shaped brain cells called astrocytes , which help keep nerve cells healthy. Brain tumors can be benign (not cancer) or malignant (cancer).

Our page on brain and spinal cord tumors has more information.

Other Types of Tumors

Germ cell tumors.

Germ cell tumors are a type of tumor that begins in the cells that give rise to sperm or eggs. These tumors can occur almost anywhere in the body and can be either benign or malignant.

Our page of cancers by body location/system includes a list of germ cell tumors with links to more information.

Neuroendocrine Tumors

Neuroendocrine tumors form from cells that release hormones into the blood in response to a signal from the nervous system. These tumors, which may make higher-than-normal amounts of hormones, can cause many different symptoms. Neuroendocrine tumors may be benign or malignant.

Our definition of neuroendocrine tumors has more information.

Carcinoid Tumors

Carcinoid tumors are a type of neuroendocrine tumor. They are slow-growing tumors that are usually found in the gastrointestinal system (most often in the rectum and small intestine). Carcinoid tumors may spread to the liver or other sites in the body, and they may secrete substances such as serotonin or prostaglandins, causing carcinoid syndrome .

Our page on gastrointestinal neuroendocrine tumors has more information.

Health Conditions

Cancer: Types, Causes, Prevention, and More

Cancer occurs when genetic mutations in abnormal cells cause them to divide rapidly. You can inherit mutations or develop them due to environmental factors.

Cancer is a large group of diseases that occur when abnormal cells divide rapidly and can spread to other tissue and organs.

These rapidly growing cells may cause tumors. They may also disrupt the body’s regular function.

Cancer is one of the leading causes of death in the world. According to the World Health Organization (WHO) , cancer accounted for almost 1 in 6 deaths in 2020. Experts are working hard to test out new cancer treatments every day.

What causes cancer?

The main cause of cancer is mutations, or changes to the DNA in your cells. Genetic mutations can be inherited. They can also occur after birth as a result of environmental forces.

These external causes, called carcinogens, can include:

physical carcinogens like radiation and ultraviolet (UV) light
chemical carcinogens like cigarette smoke, asbestos, alcohol, air pollution, and contaminated food and drinking water
biological carcinogens like viruses, bacteria, and parasites

According to the WHO , about 33 percent of cancer deaths may be caused by tobacco, alcohol, high body mass index (BMI), low fruit and vegetable consumption, and not getting enough physical activity.

Risk factors

Certain risk factors may increase your chance of developing cancer. These risk factors can include:

tobacco use
high alcohol consumption
an unhealthy diet, characterized by red and processed meat , sugary drinks and salty snacks, starchy foods, and refined carbohydrates including sugars and processed grains, according to a 2017 review
a lack of physical activity
exposure to air pollution
exposure to radiation
unprotected exposure to UV light, such as sunlight
infection by certain viruses including H. pylori , human papillomavirus (HPV) , hepatitis B , hepatitis C , HIV , and the Epstein-Barr virus , which causes infectious mononucleosis

The risk of developing cancer also increases with age. In general, the risk of developing cancer appears to increase until the age of 70 to 80 and then diminish, according to the National Cancer Institute (NCI).

A 2020 review suggests this may be the result of:

less effective cell repair mechanisms that come with aging
buildup of risk factors over the course of life
duration of exposures to carcinogens

Some existing health conditions that cause inflammation may also increase your risk of cancer. An example is ulcerative colitis, a chronic inflammatory bowel disease.

Types of cancer

Cancers are named for the area in which they begin and the type of cell they are made of, even if they spread to other parts of the body. For example, a cancer that begins in the lungs and spreads to the liver is still called lung cancer.

There are also several clinical terms used for certain general types of cancer:

Carcinoma is a cancer that starts in the skin or the tissues that line other organs.
Sarcoma is a cancer of connective tissues such as bones, muscles, cartilage, and blood vessels.
Leukemia is a cancer of the bone marrow, which creates blood cells.
Lymphoma and myeloma are cancers of the immune system.

Learn more about specific types of cancer with the resources below.

appendix cancer
bladder cancer
bone cancer
brain cancer
breast cancer
cervical cancer
colon or colorectal cancer
duodenal cancer
endometrial cancer
esophageal cancer
heart cancer
gallbladder cancer
kidney or renal cancer
laryngeal cancer
liver cancer
lung cancer
mesothelioma
oral cancers
ovarian cancer
pancreatic cancer
penile cancer
prostate cancer
rectal cancer
skin cancer
small intestine cancer
spleen cancer
stomach or gastric cancer
testicular cancer
thyroid cancer
uterine cancer
vaginal cancer
vulvar cancer

The importance of early detection

Early detection is when cancer is found in its early stages. This can increase the effectiveness of treatment and lower the mortality rate.

Cancer screenings may help detect signs of cancer early. Some common cancer screenings may detect:

Cervical cancer and prostate cancer. Some screenings, such as for cervical cancer and prostate cancer, may be done as part of routine exams.
Lung cancer. Screenings for lung cancer may be performed regularly for those who have certain risk factors.
Skin cancer. Skin cancer screenings may be performed by a dermatologist if you have skin concerns or are at risk of skin cancer.
Colorectal cancer. The American Cancer Society (ACS) recommends regular screenings for colorectal cancer beginning at age 45. These screenings are typically performed during a colonoscopy. At-home testing kits may also be able to detect some forms of colorectal cancer, according to a 2017 review of research .
Breast cancer. Mammograms to test for breast cancer are recommended for women ages 45 and older , but you may choose to begin screenings at age 40. In people at a high risk, screenings may be recommended earlier.

If you have a family history of cancer or have a high risk of developing cancer, it is important to follow a doctor’s screening recommendations.

While recognizing cancer warning signs may help people with cancer seek diagnosis and treatment, some cancers may be harder to detect early and may not show symptoms until the later stages.

Signs and symptoms of cancer can include:

lumps or growths on the body
unexplained weight loss
tiredness and fatigue
night sweats
changes in digestion
changes in skin

Specific types of cancers often have their own warning signs . If you are experiencing unexplainable symptoms, it is best to contact a doctor for a diagnosis.

How does cancer grow and spread?

Abnormal cell division.

Normal cells in your body grow and divide. Each one has a life cycle determined by the type of cell. As cells become damaged or die off, new cells take their place.

Cancer disrupts this process and causes cells to grow abnormally. It’s caused by changes or mutations in the cell’s DNA.

The DNA in each cell has instructions that tell the cell what to do and how to grow and divide. Mutations occur frequently in DNA, but usually cells correct these mistakes. When a mistake is not corrected, a cell can become cancerous.

Mutations can cause cells that should be replaced to survive instead of die, and new cells to form when they’re not needed. These extra cells can divide uncontrollably, causing tumors to form.

Creation of tumors

Tumors can cause health problems, depending on where they grow in the body.

Not all tumors are cancerous. Benign tumors are noncancerous and do not spread to nearby tissues.

But sometimes, tumors can grow large and cause problems when they press against neighboring organs and tissue. Malignant tumors are cancerous and can invade other parts of the body.

Some cancer cells can also spread through the bloodstream or lymphatic system to distant areas of the body. This is called metastasis.

Cancers that have metastasized are considered more advanced than those that have not. Metastatic cancers are often harder to treat and more fatal.

Cancer treatment can include different options, depending on the type of cancer and how advanced it is.

Localized treatment. Localized treatment usually involves using treatments like surgery or local radiation therapy at a specific area of the body or tumor.
Systemic treatment. Systemic drug treatments, such as chemotherapy, targeted therapy, and immunotherapy, can affect the entire body.
Palliative treatment. Palliative care involves relieving health symptoms associated with cancer, such as trouble breathing and pain.

Different cancer treatments are often used together to remove or destroy as many cancerous cells as possible.

The most common types of treatment are:

Surgery removes as much of the cancer as possible. Surgery is often used in combination with some other therapy in order to make sure all of the cancer cells are gone.

Chemotherapy

Chemotherapy is a form of aggressive cancer treatment that uses medications that are toxic to cells to kill rapidly dividing cancer cells. It may be used to shrink the size of a tumor or the number of cells in your body and lower the likelihood of the cancer spreading.

Radiation therapy

Radiation therapy uses powerful, focused beams of radiation to kill cancer cells. Radiation therapy done inside of your body is called brachytherapy, while radiation therapy done outside of your body is called external beam radiation.

Stem cell (bone marrow) transplant

This treatment repairs diseased bone marrow with healthy stem cells. Stem cells are undifferentiated cells that can have a variety of functions. These transplants allow doctors to use higher doses of chemotherapy to treat the cancer. A stem cell transplant is commonly used to treat leukemia.

Immunotherapy (biological therapy)

Immunotherapy uses your body’s own immune system to attack cancer cells. These therapies help your antibodies recognize the cancer, so they can use your body’s natural defenses to destroy cancer cells.

Hormone therapy

Hormone therapy removes or blocks hormones that fuel certain cancers to stop cancer cells from growing. This therapy is a common treatment for cancers that may use hormones to grow and spread, such as certain types of breast cancer and prostate cancer .

Targeted drug therapy

Targeted drug therapy uses drugs to interfere with certain molecules that help cancer cells grow and survive. Genetic testing may reveal if you are eligible for this type of therapy. It may depend on the type of cancer you have and the genetic mutations and molecular characteristics of your tumor.

Clinical trials

Clinical trials investigate new ways to treat cancer. This may include testing the effectiveness of drugs that have already been approved by the Food and Drug Administration (FDA) but for other purposes. It can also include trying new drugs. Clinical trials can offer another option for people who may have not seen the level of success they wanted with conventional treatments. In some cases, this treatment may be provided for free.

If you are interested in this kind of therapy, find clinical trials near you.

Alternative medicine

Alternative medicine may be used to complement another form of treatment. It may help decrease symptoms of cancer and side effects of cancer treatment, such as nausea, fatigue, and pain. Alternative medicine for cancer can include:

acupuncture
relaxation techniques

After you get a cancer diagnosis, your outlook can depend on a number of factors. These factors can include:

type of cancer
stage of cancer at diagnosis
location of cancer
general health

Knowing the factors that contribute to cancer can help you live a lifestyle that decreases your cancer risk.

Preventive measures to reduce your risk of developing cancer can include:

avoiding tobacco and secondhand smoke
limiting your intake of processed meats
eating a diet that focuses mainly on plant-based foods, lean proteins, and healthy fats, such as the Mediterranean diet
avoiding alcohol or drinking in moderation
maintaining a moderate body weight and BMI
doing regular moderate physical activity for 150 to 300 minutes per week
staying protected from the sun by avoiding direct sun exposure and wearing a broad spectrum sunscreen, hat, and sunglasses
avoiding tanning beds
getting vaccinated against viral infections that can lead to cancer, such as hepatitis B and HPV

Meet with a doctor regularly so they can screen you for various types of cancer. This increases your chances of catching any possible cancers as early as possible.

Cancer is a group of serious diseases that are caused by genetic changes in your cells. Abnormal cancer cells may divide rapidly and form tumors.

Risk factors like smoking, drinking alcohol, a lack of physical activity, an unhealthy diet, having a high BMI, and catching certain viruses and bacteria may contribute to developing cancer.

Screenings may help detect cancer early when it is easier to treat. The treatment plan and outlook for people with cancer can depend on the type of cancer, the stage at which it is diagnosed, and their age and general health.

How we reviewed this article:

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American Cancer Society guideline for diet and physical activity. (2020). https://www.cancer.org/healthy/eat-healthy-get-active/acs-guidelines-nutrition-physical-activity-cancer-prevention/guidelines.html
American Cancer Society recommendations for the early detection of breast cancer. (2022). https://www.cancer.org/cancer/breast-cancer/screening-tests-and-early-detection/american-cancer-society-recommendations-for-the-early-detection-of-breast-cancer.html
Amjad MT, et al. (2021). Cancer chemotherapy. https://www.ncbi.nlm.nih.gov/books/NBK564367/
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Laconi E, et al. (2020). Cancer as a disease of old age: changing mutational and microenvironmental landscapes. https://www.nature.com/articles/s41416-019-0721-1
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Malignant tumours and benign tumours

Nomenclature of benign tumours, nomenclature of malignant tumours, site of origin.

Statistical records
Preventable cancers
Cancer and age
Death rates
Variation with region and culture
Exposure to carcinogens and disease
Presentation
Precancerous stage
The noninvasive stage
Invasion and dissemination
Angiogenesis
Microinvasion
Dissemination
Effects of location
Effects of functional activity
Effects of acute events
Systemic effects of malignant tumours
Immune surveillance
Tumour-specific antigens
Tumour-associated antigens
Grading and staging
Molecular evaluation
Radiation therapy
Chemotherapy
Bone marrow transplantation
Targeted therapies
Angiogenesis inhibitors
Immunotherapy
Gene therapy
Chemoprevention
Screening and early detection
Genetic and epigenetic programs
Hallmarks of cancer cells
The role of mutation
Retroviruses and the discovery of oncogenes
Proto-oncogenes and the cell cycle
Chromosomal translocation
Gene amplification
Point mutation
Discovery of the first tumour suppressor gene
Loss of function of the RB protein
The p53 gene
Other tumour suppressor genes
DNA repair defects
Apoptosis and cancer development
Telomeres and the immortal cell
Cancer stem cells
Invasion and metastasis
Human papillomaviruses
Epstein-Barr virus
Hepatitis B virus
RNA viruses
Ultraviolet radiation
Ionizing radiation
Familial cancer syndromes
Syndromes resulting from inherited defects in DNA repair mechanisms
Milestones in cancer science

Does smoking cause lung cancer?
What are the common symptoms of lung cancer?

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cancer , group of more than 100 distinct diseases characterized by the uncontrolled growth of abnormal cells in the body.

Though cancer has been known since antiquity, some of the most significant advances in scientists’ understanding of it have been made since the middle of the 20th century. Those advances led to major improvements in cancer treatment, mainly through the development of methods for timely and accurate diagnosis , selective surgery , radiation therapy , chemotherapeutic drugs , and targeted therapies (agents designed against specific molecules involved in cancer).

Advances in treatment have succeeded in bringing about a decrease in cancer deaths, though mainly in developed countries. Indeed, cancer remains a major cause of sickness and death throughout the world. By 2018 the number of new cases diagnosed annually had risen to more than 18 million, more than half of them in less-developed countries, and the number of deaths from cancer in 2018 was 9.6 million worldwide . About 70 percent of cancer deaths were in low- and middle-income countries.

The World Health Organization (WHO) has estimated that the global cancer burden could be reduced by as much as 30 to 50 percent through prevention strategies , particularly through the avoidance of known risk factors. In addition, laboratory investigations aimed at understanding the causes and mechanisms of cancer have maintained optimism that the disease can be controlled. Through breakthroughs in cell biology , genetics , and biotechnology , researchers have gained a fundamental understanding of what occurs within cells to cause them to become cancerous. Those conceptual gains are steadily being converted into actual gains in the practice of cancer diagnosis and treatment, with notable progress toward personalized cancer medicine, in which therapy is tailored to individuals according to biological anomalies unique to their disease. Personalized cancer medicine is considered the most-promising area of progress yet for modern cancer therapy.

A Yorkshire terrier dressed up as a veterinarian or doctor on a white background. (dogs)

Tumours , or neoplasms (from Greek neo , “new,” and plasma , “formation”), are abnormal growths of cells arising from malfunctions in the regulatory mechanisms that oversee the cells’ growth and development. However, only some types of tumours threaten health and life. With few exceptions, that distinction underlies their division into two major categories: malignant or benign .

The most threatening tumours are those that invade and destroy healthy tissues in the body’s major organ systems by gaining access to the circulatory or lymphatic systems . The process of spread, accompanied by the seeding of tumour cells in distant areas, is known as metastasis . Tumours that grow and spread aggressively in this manner are designated malignant , or cancerous.

If a tumour remains localized to the area in which it originated and poses little risk to health, it is designated benign . Although benign tumours are indeed abnormal, they are far less dangerous than malignant tumours because they have not entirely escaped the growth controls that keep normal cells in check. They are not aggressive and do not invade surrounding tissues or spread to distant sites. In some cases they even function like the normal cells from which they arise. Nevertheless, though benign tumours are incapable of dissemination, they can expand and place pressure on organs, causing signs or symptoms of disease. In some cases benign tumours that compress vital structures can cause death—for instance, tumours that compress the brainstem , where the centres that control breathing are located. However, it is unusual for a benign tumour to cause death.

When the behaviour of a neoplasm is difficult to predict, it is designated as being of “undetermined malignant potential,” or “borderline.”

Tumour nomenclature

Malignant and benign are important distinctions, but they are broad categories that comprise many different forms of cancer. A more-detailed and useful way to classify and name the many kinds of tumours is by their site of origin (the cell or tissue from which a tumour arises) and by their microscopic appearance. That classification scheme, though not followed with rigid logic or consistency, allows tumours to be categorized by a characteristic clinical behaviour, such as prognosis, and by response to therapy. Tumour nomenclature based on site and tissue type thus provides a means of identifying tumours and determining the course of treatment.

Tumours may also be classified according to the genetic defects found in their cells, thanks to advances in the understanding of human genetic structure. Such classification schemes have facilitated decisions regarding course of treatment and the development of treatments that target specific genetic defects. The development of targeted agents has permitted the prescribing of more-effective and less-toxic therapies.

In the majority of cases, benign tumours are named by attaching the suffix -oma to the name of the tissue or cell from which the cancer arose. For example, a tumour that is composed of cells related to bone cells and has the structural and biochemical properties of bone substance (osteoid) is classified as an osteoma . That rule is followed with a few exceptions for tumours that arise from mesenchymal cells (the precursors of bone and muscle).

Benign tumours arising from epithelial cells (cells that form sheets that line the skin and internal organs) are classified in a number of ways and thus have a variety of names. Sometimes classification is based on the cell of origin, whereas in other cases it is based on the tumour’s microscopic architectural pattern or gross appearance. The term adenoma , for instance, designates a benign epithelial tumour that either arises in endocrine glands or forms a glandular structure. Tumours of the ovarian epithelium that contain large cysts are called cystadenomas.

When a tumour gives rise to a mass that projects into a lumen (a cavity or channel within a tubular organ), it is called a polyp . Most polyps are epithelial in origin. Strictly speaking, the term polyp refers only to benign growths; a malignant polyp is referred to as a polypoid cancer in order to avoid confusion.

Benign tumours built up of fingerlike projections from the skin or mucous membranes are called papillomas.

For the naming of malignant tumours, the rules for using prefixes and suffixes are similar to those used to designate benign neoplasms. The suffix - sarcoma indicates neoplasms that arise in mesenchymal tissues—for instance, in supportive or connective tissue such as muscle or bone. The suffix - carcinoma , on the other hand, indicates an epithelial origin. As with benign tumours, a prefix indicates the predominant cell type in the tumour. Thus, a liposarcoma arises from a precursor to a fat cell called a lipoblastic cell; a myosarcoma is derived from precursor muscle cells (myogenic cells); and squamous-cell carcinoma arises from the outer layers of mucous membranes or the skin (composed primarily of squamous, or scalelike, cells).

Just as adenoma designates a benign tumour of epithelial origin that takes on a glandlike structure, so adenocarcinoma designates a malignant epithelial tumour with a similar growth pattern. Usually the term is followed by the organ of origin—for instance, adenocarcinoma of the lung .

Malignant tumours of the blood -forming tissue are designated by the suffix -emia (Greek: “blood”). Thus, leukemia refers to a cancerous proliferation of white blood cells (leukocytes). Cancerous tumours that arise in lymphoid organs, such as the spleen , the thymus , or the lymph glands , are described as malignant lymphomas . The term lymphoma is often used without the qualifier malignant to denote cancerous lymphoid tumours; however, this usage can be confusing, since the suffix -oma , as mentioned above, more properly designates a benign neoplasm.

The suffix -oma is also used to designate other malignancies, such as seminoma, which is a malignant tumour that arises from the germ cells of the testis . In a similar manner, malignant tumours of melanocytes (the skin cells that produce the pigment melanin ) should be called melanocarcinomas, but for historical reasons the term melanoma persists.

In some instances a neoplasm is named for the physician who first described it. For example, the malignant lymphoma called Hodgkin disease was described in 1832 by English physician Thomas Hodgkin . Burkitt lymphoma is named after British surgeon Denis Parsons Burkitt ; Ewing sarcoma of bone was described by James Ewing; and nephroblastoma , a malignant tumour of the kidney in children, is commonly called Wilms tumour, for German surgeon Max Wilms.

The site of origin of a tumour, which is so important in its classification and naming (as explained above), also is an important determinant of the way a tumour will grow, how fast it will give rise to clinical symptoms, and how early it may be diagnosed. For example, a tumour of the skin located on the face is usually detected very early, whereas a sarcoma located in the deep soft tissues of the abdomen can grow to weigh 2 kg (5 pounds) before it causes much of a disturbance. The site of origin of a tumour also determines the signs and symptoms of disease that the individual will experience and influences possible therapeutic options.

The most-common tumour sites in females are the breast , the lung , and the colon . In men the most frequently affected sites are the prostate , the lung, and the colon. Each tumour site and type presents its own specific set of clinical manifestations . However, there are a number of common clinical presentations, or syndromes, caused by many different kinds of tumours.

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Cancer is a leading cause of death worldwide, accounting for nearly 10 million deaths in 2020, or nearly one in six deaths.
The most common cancers are breast, lung, colon and rectum and prostate cancers.
Around one-third of deaths from cancer are due to tobacco use, high body mass index, alcohol consumption, low fruit and vegetable intake, and lack of physical activity. In addition, air pollution is an important risk factor for lung cancer.
Cancer-causing infections, such as human papillomavirus (HPV) and hepatitis, are responsible for approximately 30% of cancer cases in low- and lower-middle-income countries.
Many cancers can be cured if detected early and treated effectively.

Cancer is a generic term for a large group of diseases that can affect any part of the body. Other terms used are malignant tumours and neoplasms. One defining feature of cancer is the rapid creation of abnormal cells that grow beyond their usual boundaries, and which can then invade adjoining parts of the body and spread to other organs; the latter process is referred to as metastasis. Widespread metastases are the primary cause of death from cancer.

The problem

Cancer is a leading cause of death worldwide, accounting for nearly 10 million deaths in 2020 (1). The most common in 2020 (in terms of new cases of cancer) were:

breast (2.26 million cases);
lung (2.21 million cases);
colon and rectum (1.93 million cases);
prostate (1.41 million cases);
skin (non-melanoma) (1.20 million cases); and
stomach (1.09 million cases).

The most common causes of cancer death in 2020 were:

lung (1.80 million deaths);
colon and rectum (916 000 deaths);
liver (830 000 deaths);
stomach (769 000 deaths); and
breast (685 000 deaths).

Each year, approximately 400 000 children develop cancer. The most common cancers vary between countries. Cervical cancer is the most common in 23 countries.

Cancer arises from the transformation of normal cells into tumour cells in a multi-stage process that generally progresses from a pre-cancerous lesion to a malignant tumour. These changes are the result of the interaction between a person's genetic factors and three categories of external agents, including:

physical carcinogens, such as ultraviolet and ionizing radiation;
chemical carcinogens, such as asbestos, components of tobacco smoke, alcohol, aflatoxin (a food contaminant), and arsenic (a drinking water contaminant); and
biological carcinogens, such as infections from certain viruses, bacteria, or parasites.

WHO, through its cancer research agency, the International Agency for Research on Cancer (IARC), maintains a classification of cancer-causing agents.

The incidence of cancer rises dramatically with age, most likely due to a build-up of risks for specific cancers that increase with age. The overall risk accumulation is combined with the tendency for cellular repair mechanisms to be less effective as a person grows older.

Risk factors

Tobacco use, alcohol consumption, unhealthy diet, physical inactivity and air pollution are risk factors for cancer and other noncommunicable diseases.

Some chronic infections are risk factors for cancer; this is a particular issue in low- and middle-income countries. Approximately 13% of cancers diagnosed in 2018 globally were attributed to carcinogenic infections, including Helicobacter pylori, human papillomavirus (HPV), hepatitis B virus, hepatitis C virus, and Epstein-Barr virus (2).

Hepatitis B and C viruses and some types of HPV increase the risk for liver and cervical cancer, respectively. Infection with HIV increases the risk of developing cervical cancer six-fold and substantially increases the risk of developing select other cancers such as Kaposi sarcoma.

Reducing the burden

Between 30 and 50% of cancers can currently be prevented by avoiding risk factors and implementing existing evidence-based prevention strategies. The cancer burden can also be reduced through early detection of cancer and appropriate treatment and care of patients who develop cancer. Many cancers have a high chance of cure if diagnosed early and treated appropriately.

Cancer risk can be reduced by:

not using tobacco;
maintaining a healthy body weight;
eating a healthy diet, including fruit and vegetables;
doing physical activity on a regular basis;
avoiding or reducing consumption of alcohol;
getting vaccinated against HPV and hepatitis B if you belong to a group for which vaccination is recommended;
avoiding ultraviolet radiation exposure (which primarily results from exposure to the sun and artificial tanning devices) and/or using sun protection measures;
ensuring safe and appropriate use of radiation in health care (for diagnostic and therapeutic purposes);
minimizing occupational exposure to ionizing radiation; and
reducing exposure to outdoor air pollution and indoor air pollution, including radon (a radioactive gas produced from the natural decay of uranium, which can accumulate in buildings — homes, schools and workplaces).

Early detection

Cancer mortality is reduced when cases are detected and treated early. There are two components of early detection: early diagnosis and screening.

Early diagnosis

When identified early, cancer is more likely to respond to treatment and can result in a greater probability of survival with less morbidity, as well as less expensive treatment. Significant improvements can be made in the lives of cancer patients by detecting cancer early and avoiding delays in care.

Early diagnosis consists of three components:

being aware of the symptoms of different forms of cancer and of the importance of seeking medical advice when abnormal findings are observed;
access to clinical evaluation and diagnostic services; and
timely referral to treatment services.

Early diagnosis of symptomatic cancers is relevant in all settings and the majority of cancers. Cancer programmes should be designed to reduce delays in, and barriers to, diagnosis, treatment and supportive care.

Screening aims to identify individuals with findings suggestive of a specific cancer or pre-cancer before they have developed symptoms. When abnormalities are identified during screening, further tests to establish a definitive diagnosis should follow, as should referral for treatment if cancer is proven to be present.

Screening programmes are effective for some but not all cancer types and in general are far more complex and resource-intensive than early diagnosis as they require special equipment and dedicated personnel. Even when screening programmes are established, early diagnosis programmes are still necessary to identify those cancer cases occurring in people who do not meet the age or risk factor criteria for screening.

Patient selection for screening programmes is based on age and risk factors to avoid excessive false positive studies. Examples of screening methods are:

HPV test (including HPV DNA and mRNA test), as preferred modality for cervical cancer screening; and
mammography screening for breast cancer for women aged 50–69 residing in settings with strong or relatively strong health systems.

Quality assurance is required for both screening and early diagnosis programmes.

A correct cancer diagnosis is essential for appropriate and effective treatment because every cancer type requires a specific treatment regimen. Treatment usually includes surgery, radiotherapy, and/or systemic therapy (chemotherapy, hormonal treatments, targeted biological therapies). Proper selection of a treatment regimen takes into consideration both the cancer and the individual being treated. Completion of the treatment protocol in a defined period of time is important to achieve the predicted therapeutic result.

Determining the goals of treatment is an important first step. The primary goal is generally to cure cancer or to considerably prolong life. Improving the patient's quality of life is also an important goal. This can be achieved by support for the patient’s physical, psychosocial and spiritual well-being and palliative care in terminal stages of cancer.

Some of the most common cancer types, such as breast cancer, cervical cancer, oral cancer, and colorectal cancer, have high cure probabilities when detected early and treated according to best practices.

Some cancer types, such as testicular seminoma and different types of leukaemia and lymphoma in children, also have high cure rates if appropriate treatment is provided, even when cancerous cells are present in other areas of the body.

There is, however, a significant variation in treatment availability between countries of different income levels; comprehensive treatment is reportedly available in more than 90% of high-income countries but less than 15% of low-income countries (3).

Palliative care

Palliative care is treatment to relieve, rather than cure, symptoms and suffering caused by cancer and to improve the quality of life of patients and their families. Palliative care can help people live more comfortably. It is particularly needed in places with a high proportion of patients in advanced stages of cancer where there is little chance of cure.

Relief from physical, psychosocial, and spiritual problems through palliative care is possible for more than 90% of patients with advanced stages of cancer.

Effective public health strategies, comprising community- and home-based care, are essential to provide pain relief and palliative care for patients and their families.

WHO response

In 2017, the World Health Assembly passed the Resolution Cancer prevention and control in the context of an integrated approach (WHA70.12) that urges governments and WHO to accelerate action to achieve the targets specified in the Global Action Plan for the prevention and control of NCDs 2013-2020 and the 2030 UN Agenda for Sustainable Development to reduce premature mortality from cancer.

WHO and IARC collaborate with other UN organizations, inlcuing the International Atomic Energy Agency, and partners to:

increase political commitment for cancer prevention and control;
coordinate and conduct research on the causes of human cancer and the mechanisms of carcinogenesis;
monitor the cancer burden (as part of the work of the Global Initiative on Cancer Registries);
identify “best buys” and other cost-effective, priority strategies for cancer prevention and control;
develop standards and tools to guide the planning and implementation of interventions for prevention, early diagnosis, screening, treatment and palliative and survivorship care for both adult and child cancers;
strengthen health systems at national and local levels to help them improve access to cancer treatments;
set the agenda for cancer prevention and control in the 2020 WHO Report on Cancer;
provide global leadership as well as technical assistance to support governments and their partners build and sustain high-quality cervical cancer control programmes as part of the Global Strategy to Accelerate the Elimination of Cervical Cancer;
improve breast cancer control and reduce avoidable deaths from breast cancer, focusing on health promotion, timely diagnosis and access to care in order to accelerate coordinated implementation through the WHO Global Breast Cancer Initiative;
support governments to improve survival for childhood cancer through directed country support, regional networks and global action as part of the WHO Global Initiative for Childhood Cancer using the Cure All approach;
increase access to essential cancer medicines, particularly through the Global Platform for Access to Childhood Cancer Medicines; and
provide technical assistance for rapid, effective transfer of best practice interventions to countries.

(1) Ferlay J, Ervik M, Lam F, Colombet M, Mery L, Piñeros M, et al. Global Cancer Observatory: Cancer Today. Lyon: International Agency for Research on Cancer; 2020 ( https://gco.iarc.fr/today , accessed February 2021).

(2) de Martel C, Georges D, Bray F, Ferlay J, Clifford GM. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health. 2020;8(2):e180-e190.

(3) Assessing national capacity for the prevention and control of noncommunicable diseases: report of the 2019 global survey. Geneva: World Health Organization; 2020.

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Published: 13 January 2020

The global challenge of cancer

Nature Cancer volume 1 , pages 1–2 ( 2020 ) Cite this article

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Cancer is a multifaceted global health issue that continues to demand action. We are launching Nature Cancer to inform, inspire and convene scientists across the multidisciplinary arena of cancer research, aiming to advance biomedical knowledge and treatment strategies within the greater framework of society.

Cancer is a disease that spans the breadth of human experience. Observed in hominid fossils and human mummies, first described in ancient times by Egyptian and later by Greek physicians, it has manifested itself throughout human history. Affecting people of all ages, cancer cuts through society, causing suffering on a global scale. According to the World Health Organization, cancer is responsible for one in six deaths, which makes it the second most common cause of death globally.

Through the ages, physicians who observed and described this disease were faced with its seeming intractability. The emergence of modern medicine changed that view through an initially slow accumulation of biological and therapeutic knowledge that accelerated with the advent of molecular cell biology and genetics in the latter part of the 20th century. This progress, together with more recent technological advances, have permitted an unprecedented understanding of the disease. Today the word ‘cancer’ refers to hundreds of distinct disease types that share similar fundamental properties. The importance of the tissue and cell type from which the disease originates is clear. It is known that the function of cancer cells at the molecular and metabolic level is crucial but is also highly context dependent. Cancer is also appreciated as a disease of change—a condition characterized by plasticity and heterogeneity, that evolves at genetic, phenotypic and pathological levels, and progresses through different stages clinically. Beyond decoding of the genetic fingerprint and molecular makeup of a specific cancer type, we understand the importance of the systemic and local tumor environment in how the disease develops and manifests. The interplay with the immune system and immune tumor microenvironment has become especially apparent in recent years. Indeed, today we recognize that cancer heterogeneity, evolution and the local and systemic environment all have key roles not only in disease development but also in the response or resistance to therapy and disease recurrence.

Technological advances such as next-generation sequencing, integrated ‘-omics’, imaging and single-cell methodologies have allowed profiling of different tumor types at a resolution and scale that were not possible previously. The ability to generate and share big data is fundamentally altering the way this disease is understood and treated—for example, by allowing the identification of biomarkers to select patients for clinical trials and evaluate therapy responses. Data science has become a core part of a field that is increasingly embracing computation, as in the form of artificial intelligence for extracting information from complex datasets. Nevertheless, the potential of such approaches to revolutionize data analysis for cancer screening, diagnosis and therapy decisions comes with challenges.

Viewing cancer as a systemic disease characterized by evolution, heterogeneity and environmental inputs may seem commonplace now, but in reality, revealing one layer of complexity only underscores other complex features that need to be appreciated. The size, quality and complexity of large datasets, such as those of The Cancer Genome Atlas, the International Cancer Genome Consortium and the Human Cell Atlas (among others), mean that considerable work is needed to decode, interpret and contextualize findings. Identifying tumor cell–intrinsic genomic and epigenomic attributes provides only a snapshot of tumor development and progression. A more complete picture may emerge with longitudinal information, as well as profiling of different cellular constituents of tumors, such as stromal and immune cells. Integrative ‘-omics’ and single-cell approaches provide the ability to do so; however, additional factors need to be considered. Among them are the peculiarities of the particular tissue and tumor type, the size and characteristics of human-participant cohorts or the choice of preclinical animal model systems, the resolution and strength of the chosen methodology and the quality of analytical tools. How data from individual patients versus larger cohorts are handled and analyzed, the information that can be obtained from each type of analysis and the extent to which tumor profiling studies may be more broadly generalizable, given the degree of inter-patient heterogeneity, are questions with which this field continues to grapple.

The developments noted above have also revolutionized the approach to treatment. The more granular understanding of cancer’s molecular drivers and tumor-cell-intrinsic or extrinsic vulnerabilities, and the addition of next-generation sequencing testing to clinical practice, have given rise to targeted therapies and the concept of precision oncology—treatment tailored to the individual patient, aiming to hit cancer-specific vulnerabilities, thereby hopefully reducing toxicities and improving quality of life for patients receiving treatment. High-throughput approaches, computational science, bioengineering and nanomedicine are changing the landscape of drug and diagnostics development. The hard-won advances in tumor immunology have led to an explosion of cancer immunotherapies. These therapeutic breakthroughs in precision medicine and immuno-oncology have successfully introduced several therapeutic modalities into the clinic. However, as with historical cancer treatments, these new modalities still encounter the setbacks of therapy resistance and lack of response, as well as their own serious adverse events. To that end, studying the fundamental mechanisms underlying these processes to devise new therapeutic strategies, and exploring innovative treatment combinations, represent major areas of focus.

An additional key consideration in the effort against cancer is the influence of the environment, daily habits and culture. We are gaining a better understanding of these facets of the disease, but such factors are often difficult to quantify and control in a real-world setting, or to model in the laboratory. The often late-stage presentation, and therefore late diagnosis, of the disease continues to hamper therapy options, and metastasis remains a major cause of cancer deaths and a main focus of foundational cancer research. Socioeconomic factors lend an additional, devastating dimension: according to the World Health Organization, 70% of cancer deaths occur in low- or middle-income countries, but even in high-income societies, certain parts of the population bear a disproportionate burden of suffering. A large fraction of cancer cases and deaths may be preventable with greater epidemiological and mechanistic understanding of environmental and behavioral risk factors. The development and wider adoption of the Pap test and HPV vaccines against cervical cancer are singular successes that exemplify the importance of early detection and prevention in neutralizing the threat of cancer in a broad population. However, this remains a disease of disparities. Therefore, it is essential to deepen our appreciation of the underlying causes of these inequalities and to work toward reversing them, always keeping the patient at the forefront of the cross-disciplinary scientific endeavor in this field. Developing more-effective screening and diagnostic means and working toward providing accessible and affordable high-quality cancer care for the wider population will be essential for addressing cancer-health disparities.

It has been thousands of years since the ancient Greek physician Hippocrates strove to understand this disease and named it ‘cancer’ from the Greek word karkinos , meaning ‘crab’, possibly as an allusion to the blood vessels emanating from tumors. We are now in the enviable position of having a much more refined understanding of the disease and we know that cancer has no panacea. Instead, it requires synthesis of knowledge, collaboration between fields and a deeper appreciation of the challenges facing patients, clinicians and scientists from different disciplines. Fortunately, this is an era of thriving biomedical research that has seen the field of cancer research expand into a vibrant, multidisciplinary community that seeks new and innovative ways to engage collectively and to tackle this disease.

As we launch Nature Cancer , we seek to provide a unique forum that embraces the breadth of this community, from foundational preclinical science to translational and clinical work. Through our pages, we aim to increase the knowledge of cancer formation, development and progression, to explore innovative approaches to cancer diagnosis, treatment and prevention, and to understand the societal impact of this disease. Ultimately, our goal is to become a point of convergence for scientists from diverse fields and to lend a new voice to discussing and contextualizing the most exciting findings and pressing issues in cancer research today. Our inaugural issue encapsulates the diversity of science we aim to bring to you and the conversations we seek to start. As we realize our first steps into this field, we thank our authors and referees and welcome our readers.

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Home — Essay Samples — Nursing & Health — Cancer — Cancer: Types, Causes, Effects and Treatment

Cancer: Types, Causes, Effects and Treatment

Categories: Cancer Therapy

About this sample

Words: 2465 |

13 min read

Published: Mar 18, 2021

Words: 2465 | Pages: 5 | 13 min read

Introduction, common causes of cancer, traditional treatments for cancer/effects, success rates for different treatments, role of mutations, breast cancer, brain cancer, lung cancer, immune system.

Allison, J., 2017. MD Anderson Cancer center. [Online] Available at: https://www.mdanderson.org/newsroom/md-anderson-immunologist-jim-allison-awarded-nobel-prize.h00-159228090.html
American cancer society , 2016 . Survival rates for breats cancer. [Online] Available at: https://www.cancer.org/cancer/breast-cancer/understanding-a-breast-cancer-diagnosis/breast-cancer-survival-rates.html
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Anon., 2018. Explination of cancer. [Online] Available at: https://www.bing.com/videos/search?q=explination+on+cancer+&view=detail&mid=94D3CB9CF0AA232DC98394D3CB9CF0AA232DC983&&FORM=VRDGAR
CTCA, 2019. CancerCompass. [Online] Available at: https://www.cancercompass.com/cancer-treatment/radiation-therapy.htm
Farlex, 2019. definition of screening. [Online] Available at: https://medical-dictionary.thefreedictionary.com/screening
R.News, 2016. R. News. [Online] Available at: https://www.rnews.co.za/article/16673/the-reality-of-breast-cancer-treatment-cost-in-south-africa
Tutor, C., 2018. cancer vs Immune system. [Online] Available at: https://www.bing.com/videos/search?q=immune+system+verses+cancer&&view=detail&mid=9524B15F2F0CE060F0739524B15F2F0CE060F073&&FORM=VRDGAR
U.S department of health, 2018. National cancer Institution. [Online] Available at: https://www.cancer.gov/about-cancer/understanding/what-is-cancer

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Essay on Cancer Treatment (For Medical Students) | Types | Diseases | Biology

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Are you looking for an essay on ‘Cancer Treatment’? Find paragraphs, long and short essays on ‘Cancer Treatment’ especially written for college and medical students.

1. Essay on Cancer Treatment: (Around 200 Words)

Success of Cancer Treatments:

The success rates for current cancer treatments are strongly influenced by the stage at which the disease is diagnosed. When cancer is detected early and tumor cells are still localized to their initial site of origin, cure rates tend to be very high, even for cancers that would otherwise have a poor prognosis (Figure 1).

Unfortunately, many cancers are difficult to detect in their early stages and by the time they are diagnosed, metastasis may have already occurred. If cancers were routinely detected at an earlier stage, many cancer deaths could be prevented.

Early detection is a feasible goal because despite the common perception that cancer arises rapidly and with little warning, most cancers develop slowly and only become aggressive and invasive after the gradual passage of time (usually measured in years rather than weeks or months). A prolonged window of opportunity therefore exists for detecting the disease in its earlier stages when treatments are more likely to be effective.

2. Essay on Cancer Treatment: (Around 350 Words)

Cancer has Few Symptoms that Arise Early or are Specific for the Disease:

The first thing to signal the presence of a disease is usually some type of physical symptom that prompts a visit to a doctor and helps guide the diagnosis. Few generalizations are possible about the symptoms of cancer because it can arise almost anywhere in the body.

When a cancer grows beyond a tiny localized clump of cells into a larger mass that invades surrounding tissues, symptoms may begin to be triggered as the tumor impinges on surrounding structures and organs.

For example, if a tumor presses on a nerve it may cause pain, or it might disrupt blood vessels and cause bleeding. The location of symptoms varies widely, depending on the type of cancer involved. After a cancer has metastasized, symptoms may appear in other parts of the body and, in some cases, may represent the first signs of disease.

Tumors tend to produce few or no symptoms when they are small and localized, so it is difficult to come up with reliable guidelines to help people detect cancer early.

For many years, the American Cancer Society publicized a list of seven warning signs that are possible indicators of the presence of cancer:

1. Change in bowel or bladder habits.

2. A sore that does not heal.

3. Unusual bleeding or discharge.

4. Thickening or lump in the breast or elsewhere.

5. Indigestion or difficulty swallowing.

6. Obvious change in a wart or mole.

7. Nagging cough or hoarseness.

Any of the preceding symptoms might be a sign of cancer, but the list has two shortcomings that limit its usefulness. First, when one of these symptoms does arise because of cancer, it may not appear until the disease has advanced to a relatively late stage.

Second, none of the listed symptoms is specific for cancer, and in most cases a person exhibiting one or more of the symptoms will not actually have cancer. Yet despite these shortcomings, each warning sign in the list indicates a condition that should be assessed by a doctor because if it does signal the presence of cancer, the outcome will be much better if treatment is started early.

3. Essay on Cancer Treatment : (Around 480 Words)

Cancer Diagnosis Includes Information Regarding the Stage of the Disease:

The verdict that cancer is present is only the beginning of a complete cancer diagnosis. One of the next issues that needs to be addressed is the question of how far a person’s cancer has progressed.

Tumor staging uses three main criteria to establish a stage number that reflects how early a cancer has been detected:

(1) The size of the primary tumor and the extent of its spread into nearby tissues,

(2) The extent to which cancer cells have spread to regional lymph nodes, and

(3) The extent to which distant metastases are evident. A low stage number means that a cancer has been caught earlier and that treatment is more likely to be successful.

Sometimes a biopsy reveals tissue abnormalities that occur even earlier, prior to the formation of an actual tumor. For example, the development of cancer in some tissues is preceded by a distinct period of dysplasia (abnormal cell proliferation accompanied by the loss of normal tissue organization).

Areas of dysplasia may revert back to normal behavior, or the abnormalities can become more severe and gradually develop into cancer. Dysplasia is a common condition in the uterus, where it is often discovered when the uterine cervix is biopsied after an abnormal Pap smear.

The conversion of dysplasia into cancer typically requires several years, providing a significant “window of opportunity” during which the dysplastic region can be removed or destroyed to prevent cancer from arising. Even when the condition is not diagnosed until carcinoma in situ has developed, these pre-invasive tumors are relatively easy to treat because they have not yet begun to invade and spread.

A slightly different sequence of precancerous stages has been uncovered by screening tests for colon cancer. Colonoscopy sometimes reveals the presence of colon polyps that, upon microscopic examination, turn out to be adenomas (benign tumors of gland cells).

The cells in a polyp can acquire subsequent mutations, usually over a period of several years, that convert the polyp first into a localized, preinvasive adenocarcinoma (carcinoma in situ) and then into an invasive adenocarcinoma.

In other words, a benign tumor is often the first step on the road to malignancy in the colon. Removal of polyps while they are still benign is therefore an effective way of decreasing a person’s risk of developing colon cancer.

The preceding examples reinforce a point that cancer arises through a multistep process that begins with early cellular abnormalities, such as dysplasia or benign neoplasia, followed by conversion into a preinvasive cancer that progresses into an invasive cancer that eventually metastasizes.

The initial stages of this process usually take a significant amount of time, providing ample opportunity for early diagnosis and treatment. When caught at any stage prior to the onset of invasion and metastasis, the disease can almost always be treated successfully.

4. Essay on Cancer Treatment: (Around 700 Words)

Cancer Diagnosis Includes Information Regarding the Microscopic Appearance and Molecular Properties of the Tumor Cells :

The diagnosis that a person has cancer is generally accompanied by information concerning the cancer’s site of origin and the cell type involved. The site of origin may or may not be the site in which the cancer was initially detected.

For example, cancer discovered in the bones of the spinal column might turn out to be lung cancer that has metastasized to bone, or cancer discovered in the liver might turn out to be stomach cancer that has metastasized to the liver.

The type of cancer in such situations is always defined by the location of the primary tumor. In other words, lung cancer that has metastasized to bone is still lung cancer, not bone cancer, and stomach cancer that has metastasized to the liver is stomach cancer, not liver cancer. Knowing the site of origin is important because it determines the type of cancer and provides information as to how the cancer is likely to behave and how it should be treated.

After a tumor’s site of origin has been determined, additional information can be provided by microscopic examination of the biopsy specimen to determine the exact type of cells involved.

For example, there are different types of lung cancer, different types of stomach cancer, and different types of skin cancer, each determined by the identity of the cell type that has become malignant. Knowing the cell type, like knowing the site of origin, provides information regarding likely tumor behavior and guidance as to the most appropriate treatment.

For cancers arising in the same site and involving the same cell type, further distinctions can be made based on the severity of the abnormalities that are observed during microscopic examination of the biopsy specimen.

Pathologists have devised systems for tumor grading in which cancers of the same type assigned different numerical grades are based on the extent of the cellular and tissue disruptions that are seen with a microscope. Lower-grade cancers have a more normal appearance and often a better prognosis for long-term survival than do higher-grade cancers.

Biochemical tests for molecular components can further refine the picture regarding likely tumor behavior and appropriate treatment strategies. For example, breast cancer specimens are often tested for the presence of estrogen receptors, which are protein molecules involved in the mechanism by which estrogen stimulates the proliferation of breast cells. Breast cancers that possess estrogen receptors tend to have a better prognosis than cancers without estrogen receptors and are more likely to respond to hormone therapies.

Cancer cells also exhibit numerous changes in gene expression that can provide information about how tumors are likely to behave. One widely used approach for measuring gene expression is DNA microarray analysis, a technique which can monitor the activity of thousands of genes simultaneously.

Experiments involving DNA micro- arrays have led to the identification of differing patterns of gene expression among tumors of the same type that allow predictions to be made regarding tumor behavior. In the case of breast cancer, for example, the expression of 21 key genes turns out to be a good indicator of whether a given tumor is likely to metastasize.

Based on this discovery, a test called Oncotype DX has been devised that measures the activity of these 21 genes and converts the data into a single number called a recurrence score.

As shown in Figure 6, women with breast cancer whose tumors have a high recurrence score are more likely to develop metastases than are women whose tumors exhibit a low recurrence score. Such information is useful in guiding treatment strategies because patients with higher recurrence scores derive more benefit from subsequent chemotherapy.

People diagnosed with cancer have a variety of treatment options available that depend both on the type of cancer they have and how far it has spread. The ultimate goal of traditional cancer treatments is the complete removal or destruction of cancer cells accompanied by minimal damage to normal tissues.

This goal is usually pursued through a combination of surgery (when possible) to remove the primary tumor, followed (if necessary) by radiation, chemotherapy, or both to destroy any remaining cancer cells.

5. Essay on Cancer Treatment: (Around 650 Words)

Surgery can Cure Cancers when they have not yet Metasized :

Surgical techniques for removing tumors were first described more than three thousand years ago, making surgery the oldest approach for treating cancer. Its early use, however, was severely limited by the excruciating pain caused in the absence of anesthetics and by the extremely high death rate from infections.

The modern era of surgery was ushered in by the discovery of ether anesthesia in the 1840s and by the introduction of carbolic acid to inhibit bacterial infections in the 1860s. By 1890, these innovations had made it possible to perform the first mastectomy—that is, complete removal of the breast in women with breast cancer.

This milestone was followed in the early 1900s by the development of surgical techniques for removing tumors from virtually every organ of the body.

When people think of cancer surgery, they usually picture a doctor using a scalpel to cut out the tumor and perhaps surrounding tissues. Although that is certainly the most common surgical technique, a variety of newer procedures using different types of instruments have broadened the concept of what surgery is.

For example, laser surgery utilizes a highly focused beam of laser light to cut through tissue or to vaporize certain cancers, such as those occurring in the cervix, larynx (voice box), liver, rectum, or skin. Electro surgery, which involves high- frequency electrical current, is sometimes used to destroy cancer cells in the skin and mouth. Cryosurgery involves the use of a liquid nitrogen spray or a very cold probe to freeze and kill cancer cells.

This technique is utilized for the treatment of certain prostate cancers and for precancerous conditions of the cervix such as dysplasia. Finally, high-intensity focused ultrasound (HIFU) is a technique that focuses acoustic energy at a selected location within the body, where the absorbed energy heats and destroys cancer cells with minimum damage to surrounding tissues.

When cancer is diagnosed before a primary tumor has spread to other sites, surgical removal of a tumor can usually cure the disease. In fact, most cancer cures are achieved in this way. But cancers arising in internal organs are difficult to detect in their early stages and have often metastasized by the time they are diagnosed.

Sometimes the metastatic tumors formed at distant sites are large enough to also be detected and surgically removed; in other cases, the body has simply been seeded with tiny clumps of cancer cells, known as micrometastases that are too small to be detected.

Because roughly half of all cancers (excluding skin cancers) have started to metastasize by the time they are diagnosed, surgical removal of the primary tumor is frequently followed by radiation, chemotherapy, or both to attack any disseminated cells that were not removed during surgery.

The growing use of follow-up radiation and chemotherapy has allowed surgeons to decrease the amount of surgery they need to perform on the average cancer patient. For example, the standard treatment for breast cancer between 1900 and 1970 was the radical mastectomy, a drastic and disfiguring operation that involves complete surgical removal of the breast along with the underlying chest muscles and lymph nodes of the armpit.

However, radical mastectomies are rarely performed today because such extensive tissue removal has not been found to improve survival compared to less drastic procedures. From 1970 to 1990 the most common procedure was the modified radical mastectomy, which involves removal of the breast and lymph nodes but not the chest muscles.

Today more than half of all breast cancer patients are treated by partial mastectomy (lumpectomy), which removes just the tumor and a small amount of surrounding normal tissue. Surgery is usually followed by radiation therapy to the breast to destroy any cancer cells that may remain in the area.

6. Essay on Cancer Treatment: (Around 400 Words)

Radiation Therapy Kills Cancer Cells by Triggering Apoptosis or Mitotic Death :

If a tumor has invaded into surrounding tissues and possibly metastasized to distant sites, surgery may not be able to remove all cancer cells from the body. In some cases, surgery is not even practical.

For example, the location of a brain tumor may make it impossible to remove the tumor without causing unacceptable brain damage, and leukemias cannot be treated surgically because the cancer cells reside mainly in the bloodstream. When surgery is insufficient by itself or impractical, other treatments are used (often after surgery) to destroy any cancer cells that may still reside in the body.

One type of treatment is radiation therapy, which uses high-energy X-rays or other forms of ionizing radiation to kill cancer cells. Ionizing radiation removes electrons from water and other intracellular molecules, thereby generating highly reactive free radicals that attack DNA. The resulting DNA damage can actually cause cancer to arise.

Ironically, the same type of radiation is used in higher doses to kill cancer cells in people who already have the disease. Radiation treatments do create a small risk that a second cancer will develop in the future, but the risk is far outweighed by the potential benefit of curing a cancer that already exists.

High doses of radiation kill cancer cells in two different ways. First, DNA damage caused by the radiation treatment activates the p53 signaling pathway, which triggers cell death by apoptosis. Lymphomas and cancers arising in reproductive tissues are particularly sensitive to this type of radiation-induced apoptosis.

However, more than half of all human cancers have mutations that disable the p53 protein or other components of the p53 signaling pathway. As a consequence, p53-induced apoptosis plays only a modest role in the response of most cancers to radiation treatment.

Radiation also kills cells by causing chromosomal damage that is so severe that it prevents cells from progressing through mitosis, and the cells die while trying to divide. Because this process of mitotic death only occurs at the time of cell division, cells that divide more frequently are more susceptible to mitotic death than cells that divide less frequently (or are not dividing at all).

This difference in susceptibility makes rapidly growing cancers more sensitive to the Killing effects of radiation than slower-growing cancers and also helps protect non-dividing or slowly dividing normal cells in the surrounding tissue from being killed by the radiation.

7. Essay on Cancer Treatment: (Around 750 Words)

Radiation Treatments are Designed to Minimize Damage to Normal Tissues :

To minimize damage to normal tissues, radiation treatments must be accurately focused on those regions of the body that contain tumor cells. This goal, called radiation planning, is accomplished by taking X-ray pictures that define the three-dimensional boundaries of the tumor and then using that information to guide a moving beam of high-energy radiation that is directed toward the target region from a number of different angles. Such an approach allows maximum radiation to be directed at the tumor area with minimal exposure to surrounding tissues.

The effectiveness of radiation therapy is determined to a large extent by differences in the survival rates of normal versus cancer cells after irradiation. If the difference in survival rates is small and the entire radiation dose is administered as a single treatment, the survival curves will closely track one another and there will be little difference in the numbers of cancer cells and normal cells killed (Figure 7, left).

It might be possible to destroy a tumor this way, but it would be at the expense of a large amount of damage to normal tissue. If the same total amount of radiation is administered as a series of lower doses, however, small differences in the survival rates of normal and cancer cells after each treatment become magnified as the treatments are repeated multiple times (see Figure 7, right).

By the end of the series of treatments, all cancer cells could be destroyed while maintaining enough normal cells to avoid serious tissue damage. For this reason, radiation therapy is usually divided into multiple treatments administered over several weeks or months.

An alternative approach for minimizing damage to normal tissues, called brachytherapy, uses a radiation source that can be inserted directly within (or close to) the tumor. For example, early stage prostate cancer is sometimes treated by implanting small radioactive pellets, about the size of a grain of rice, directly into the prostate gland.

The pellets emit low doses of radiation for weeks or months and are simply left in place after the radiation has all been emitted. The advantage of this approach is that most of the radiation is concentrated in the prostate gland itself, sparing surrounding tissues such as the bladder and rectum.

Another technique for improving the effectiveness of radiation therapy involves agents that sensitize tumor cells to the killing effects of radiation. One group of drugs, known as hypoxic radio sensitizers, mimic oxygen and are taken up by cancer cells, which frequently tend to be hypoxic (deficient in oxygen).

Radiation creates more cellular damage in the presence of adequate oxygen, so the uptake of these drugs by cancer cells increases the effectiveness of radiation therapy. Combining radiation treatments with certain anticancer drugs, such as fluorouracil and platinum compounds, can likewise enhance the effectiveness of radiation treatments. The properties of these and related anticancer drugs will be described shortly, when we discuss the topic of cancer chemotherapy.

Raising the temperature of tumor tissue by a few degrees—a technique known as hyperthermia—also sensitizes cells to the killing effects of radiation. Hyperthermia even works when it is administered after radiation treatment, suggesting that the heat may be interfering with cellular repair pathways.

The combination of radiation and hyperthermia is most effective for tumors that are located in relatively accessible regions of the body, where the applied heat can thoroughly penetrate the tumor tissue. The main difficulty with this approach is finding ways of applying heat to hard-to-reach tumors located deep inside the body.

Radiation therapy is associated with various side effects that limit the dose of radiation that can be safely administered. The most serious problems arise in tissues containing large numbers of normal dividing cells, which are also susceptible to radiation-induced killing. For example, radiation damage to the dividing cells that line the gastrointestinal tract causes nausea, vomiting, and diarrhea.

And damage to dividing cells in the bone marrow reduces the production of one or more types of blood cells, which can lead to anemia, defective blood clotting, and immune deficiencies that increase the susceptibility to infections. The likelihood that such side effects will be severe depends to a great extent on the location of the tumor and its sensitivity to radiation-induced killing.

Some cancers are very sensitive to radiation and can be destroyed with modest doses that elicit minimal side effects, whereas other cancers require high radiation doses and are more difficult to control using radiation (Table 1).

8. Essay on Cancer Treatment: (Around 230 Words)

Chemotherapy Involves the Use of Drugs that Circulate in the Bloodstream to reach Cancer Cells Wherever they may Reside :

The third main approach for treating cancer (in addition to surgery and radiation) is chemotherapy, which involves the use of drugs that either kill cancer cells or interfere with the ability of cancer cells to proliferate.

Chemotherapy is especially well suited for treating cancers that have already metastasized because drugs circulate through the bloodstream to reach cancer cells wherever they may have spread, even if the metastasizing cells have not yet formed visible tumors. This also means, however, that the toxic side effects commonly associated with chemotherapy can occur anywhere in the body because most anticancer drugs, like radiation, are toxic to dividing cells in general.

Despite its various side effects, chemotherapy has been successfully applied to a wide range of cancers. In some cases, as with certain forms of leukemia, chemotherapy may cure cancer by itself. More commonly, chemotherapy is employed in conjunction with surgery, radiation, or both.

Dozens of anticancer drugs are currently available and the best choice will vary, depending on the type and stage of the cancer being treated. Based on differences in the way they work, the various drugs can be grouped into several distinct categories (Table 2).

In the following sections , each category will be discussed in turn:

9. Essay on Cancer Treatment: (Around 600 Words)

Antimetabolites Disrupt DNA Synthesis by Substituting for Molecules Involved in Normal Metabolic Pathways :

Antimetabolites, the first group of chemotherapeutic drugs that we will consider, are molecules that resemble substances involved in normal cellular metabolism. This resemblance causes enzymes to bind to antimetabolites in place of the normal molecules, thereby disrupting essential metabolic pathways and poisoning the cell. Most of the antimetabolites used in cancer chemotherapy disrupt pathways required for normal DNA synthesis and repair.

The use of this approach for treating cancer was pioneered in the 1940s by Sidney Farber, who had been studying the nutritional needs of children with leukemia. Farber initially believed that vitamin therapy might help children fight off the disease, so he provided them with supplements of various vitamins, including the B vitamin, folic acid.

Unexpectedly, the added folic acid made the leukemias grow even faster. While that was certainly not the desired result, it raised an intriguing possibility: If cancer growth is stimulated by excess folic acid, blocking the action of folic acid might have the opposite effect and restrain the disease.

Farber therefore decided to treat some of his patients with folic acid analogs, which are chemical derivatives of folic acid that can substitute for the natural molecule and thereby disrupt any pathways in which folic acid is normally involved. When one analog, called aminopterin, was given to several children who were very sick with leukemia, the children quickly regained their health and returned to virtually normal lives.

Unfortunately, the improvement turned out to be only temporary, but these transient remissions caused a stir of excitement and stimulated the hunt for other antimetabolites whose effects might be more permanent than those of aminopterin.

The resulting search led to the discovery of methotrexate, a derivative of folic acid that efficiently binds to and inhibits the enzyme dihydrofolate reductase (Figure 8). Dihydrofolate reductase catalyzes the production of a reduced form of folic acid that is required for the synthesis of several bases found in DNA; inhibition of dihydrofolate reductase by methotrexate therefore disrupts pathways involved in DNA synthesis and repair.

Shortly after its discovery, methotrexate was shown to be an effective treatment for choriocarcinoma, a cancer arising from cells of the placental membranes that are sometimes left behind after childbirth. Choriocarcinoma was fatal for most women who developed the disease prior to the introduction of methotrexate chemotherapy in the mid-1950s.

After methotrexate began to be used, cure rates improved to almost 90%. Although its effects are not always this dramatic, methotrexate is currently used to treat a diverse spectrum of cancers, including acute leukemias and tumors of the breast, bladder, and bone.

In addition to analogs of folic acid such as methotrexate, analogs of the nitrogenous bases found in DNA are also useful for cancer chemotherapy.

DNA contains two types of bases: single-ring compounds called pyrimidines, which include the bases cytosine (C) and thymine (T); and double-ring compounds called purines, which include the bases adenine (A) and guanine (G).

Several analogs of pyrimidines and purines are routinely used as anticancer drugs. Examples include the pyrimidine analogs fluorouracil and cytarabine (also called cytosine arabinoside) and the purine analogs mercaptopurine and thioguanine.

As shown in Figure 9, the close resemblance of these substances to normal bases found in DNA causes the analogs to bind to and thereby disrupt the activity of enzymes involved in DNA synthesis and repair. Pyrimidine and purine analogs are used mainly for treating leukemias and lymphomas, although fluorouracil is effective against a broad spectrum of other cancers as well.

10. Essay on Cancer Treatment: (Around 650 Words)

Alkylating and Platinating Drugs Act by Crosslinking DNA:

Alkylating agents are highly reactive organic molecules that trigger DNA damage by linking themselves directly to DNA. This ability to attack DNA molecules makes alkylating agents mutagenic as well as carcinogenic.

However, alkylating agents are also employed as anticancer drugs because they kill cancer cells at higher doses, and the risk that they may cause cancer in such cases is outweighed by the potential benefit of curing a cancer that already exists.

The first alkylating agent to be employed for cancer chemotherapy has an interesting history. During World War I, the German military used an oily alkylating agent called sulfur mustard as a chemical weapon because it vaporizes easily and causes severe blistering injuries to the skin and lungs. A more toxic version, called nitrogen mustard, was produced and stockpiled by both Germany and the United States during World War II.

Nitrogen mustard was never employed on the battlefield, but German bombers attacked an Italian seaport in 1943 and sank a U.S. supply ship loaded with 100 tons of weapons containing the toxic chemical. Survivors pulled from the water, which had become heavily contaminated with nitrogen mustard, exhibited severe skin burns and quickly developed a variety of internal symptoms, including a dramatic drop in the number of blood lymphocytes.

Given this toxic effect on lymphocytes, scientists at Yale University decided to investigate whether nitrogen mustard would have a similar effect on cancers arising from lymphocytes. Shortly after the end of World War II, they reported that nitrogen mustard injections cause lymphocytic cancers to regress in animals and humans— the first demonstration of the potential usefulness of alkylating agents as anticancer drugs.

Better alkylating agents have subsequently been developed, but nitrogen mustard (now called mechlorethamine) is still occasionally used to treat Hodgkin’s lymphoma. Medical staffs who handle the drug take precautions to avoid inhaling the vapors of this one-time chemical weapon and must be certain that it is injected cleanly into a patient’s vein without contacting the skin.

Based on the initial promising results with nitrogen mustard, hundreds of other alkylating agents have been synthesized in the laboratory and tested in animals for anticancer activity. This effort has produced several drugs related to nitrogen mustard, including cyclophosphamide, chlorambucil, and melphalan that are routinely used to treat cancer patients.

In addition to substances related to nitrogen mustard, other alkylating agents have been developed for use as anticancer drugs, including thiotepa and nitrosourea compounds, such as BCNU (bischloroethyl nitrosourea). In general, the various alkylating agents disrupt normal DNA function by crosslinking the two strands of the DNA double helix (Figure 10, top). As a result, the two strands are unable to separate and DNA replication cannot take place, thereby preventing cell division.

Another group of DNA-crosslinking agents used in cancer chemotherapy contain the element platinum (see Figure 10, bottom). The ability of these substances, called platinating agents, to act as anticancer drugs was discovered in a roundabout manner. In some experiments performed during the 1960s that were totally unrelated to cancer biology, platinum electrodes were used to pass an electric current through a culture of bacterial cells to see how the cells react to electricity.

The bacteria stopped dividing, but it was soon discovered that this response was caused not by the electricity but by an unexpected reaction involving the platinum electrodes. In essence, ammonium chloride present in the culture medium had reacted with platinum in the electrodes to form a nitrogen-containing platinum compound called cisplatin, which in turn inhibited bacterial cell division.

The ability of cisplatin to block cell division led to successful tests on cancer cells, and the drug was approved for trials in human cancer patients in 1972. Cisplatin (trade name Platinol) is now one of the most effective agents in our arsenal of anticancer drugs, and efforts are being made to synthesize derivatives of cisplatin that might work even better.

11. Essay on Cancer Treatment: (Around 400 Words)

Antibiotics and Plant-Derived Drugs are Two Classes of Natural Substances Used in Cancer Chemotherapy :

Most of the antimetabolites and alkylating agents being used as anticancer drugs are synthetic molecules that were created in the laboratory for the purpose of treating cancer. Over the centuries, humans have also found ways of treating disease by drawing on natural substances produced by living organisms.

An especially dramatic twentieth-century example was the discovery of penicillin, a substance produced by a fungus that turned out to be one of the first effective drugs against bacterial infections.

Penicillin is an antibiotic, a term that refers to any substance produced by a microorganism, or a synthetic derivative, that kills or inhibits the growth of other microorganisms or cells. Antibiotics are generally thought of as being antibacterial drugs, but some of them exhibit anticancer properties as well.

One of the most fruitful sources of antibiotics for cancer chemotherapy has been a group of bacteria called Streptomyces. Besides producing streptomycin, which is an antibiotic used for treating tuberculosis and other serious bacterial infections, members of the Streptomyces group synthesize several antibiotics that have found their way into our arsenal of anticancer drugs, including doxorubicin, daunorubicin, mitomycin, and bleomycin.

All these antibiotics target the DNA molecule, although their mechanisms of action are somewhat different. Doxorubicin and daunorubicin insert themselves into the DNA double helix and inhibit the action of topoisomerase, an enzyme that normally breaks and rejoins DNA strands during DNA replication to prevent excessive twisting of the double helix. In contrast, mitomycin is a DNA crosslinking agent and bleomycin triggers DNA strand breaks.

Plants are another natural source of anticancer drugs. Several of the drugs obtained from plants act as topoisomerase inhibitors; included in this category are etoposide and teniposide, derived from a substance present in the mayapple (mandrake) plant, and topotecan and irinotecan, derived from a substance present in the bark of the Chinese camptotheca tree.

Another group of plant- derived drugs attack the microtubules that make up the mitotic spindle. This class of drugs includes vinblastine and vincristine, obtained from the Madagascar periwinkle plant and Taxol (generic name paclitaxel), discovered in the bark of the Pacific yew tree.

Vinblastine and vincristine block the process of microtubule assembly, whereas Taxol stabilizes microtubules and promotes the formation of abnormal microtubule bundles. In either case, the mitotic spindle is disrupted and cells cannot divide.

12. Essay on Cancer Treatment: (Around 700 Words)

Hormones and Differentiating Agents are Relatively Nontoxic Tools for Halting the Growth of Certain Cancers :

One of the main problems with the drugs described thus far is that their toxic effects on DNA replication and cell division are harmful to normal cells as well as to cancer cells. When cancers arise in hormone-dependent tissues, an alternative and considerably less toxic approach can sometimes be used.

This approach, known as hormone therapy, was pioneered in the 1940s by Charles Huggins in studies involving prostate cancer patients. Based on earlier observations in animals, Huggins believed that the proliferation of prostate cells is dependent on steroid hormones known as androgens (testosterone is one example).

In an effort to eliminate the source of androgens in men with advanced prostate cancer, he surgically removed their testicles, which produce most of the testosterone, and also treated them with the female steroid hormone, estrogen. More than half of his prostate cancer patients improved and saw their tumor growth reduced.

These early observations eventually led to the development of drugs that block the production or the actions of androgens as an alternative to removing the testicles. Androgen production is normally controlled by peptide hormones called gonadotropins, which are synthesized in the pituitary gland.

One drug used to treat prostate cancer, named leuprolide, is an analog of the gonadotropin-releasing hormone that controls the release of these gonadotropins. By suppressing the release of gonadotropins, leuprolide inhibits androgen production by the testicles.

Another group of drugs inhibit the activity of androgen receptors, which are receptor proteins located in prostate epithelial cells that bind incoming androgens and transmit the signal that stimulates cell division. Flutamide and bicalutamide are examples of anticancer drugs that act by blocking androgen receptors.

Similar considerations apply to breast cancers, which arise from cells whose normal proliferation is driven by steroid hormones of the estrogen family. For breast cancers that retain this estrogen requirement, drugs that block estrogen action may be effective cancer treatments. One widely used drug that works in this way is tamoxifen, a molecule that exhibits some similarities to estrogen in chemical structure (Figure 11).

Estrogens normally exert their effects on target cells by binding to intracellular proteins called estrogen receptors. When tamoxifen is administered to breast cancer patients whose tumors require estrogen, it binds to estrogen receptors in place of estrogen and prevents the receptors from being activated. Another group of drugs, called aromatase inhibitors, inhibit one of the enzymes required for estrogen synthesis.

Generally these drugs are only recommended for treating breast cancer in postmenopausal women, where they inhibit the synthesis of the small amounts of estrogen that are being produced.

A somewhat different rationale is used when applying the principle of hormone therapy to lymphocytic cancers. The adrenal cortex produces a family of steroid hormones called glucocorticoids, whose properties include the ability to inhibit lymphocyte proliferation. Consequently prednisone, a synthetic glucocorticoid that slows down the proliferation of lymphocytes, is sometimes used in treating lymphomas and lymphocytic leukemias.

One advantage of hormone therapies is that their side effects tend to be mild because they do not destroy normal cells and because they only affect a selected group of target cells whose proliferation is controlled by the hormone in question. On the other hand, this latter property also imparts a significant limitation: Hormone-based treatments are only useful for cancers that arise in hormone-dependent tissues.

And even in these tissues, cancers do not always exhibit the hormone-dependence seen in the corresponding normal cells. For example, some breast cancers lack the estrogen receptors found in normal breast cells, and some prostate cancers lack the androgen receptors found in normal prostate cells. In such cases, hormone therapies are of little value.

Another relatively nontoxic approach to cancer chemotherapy involves the use of substances called differentiating agents. Whereas hormone therapies are designed to restrain cell proliferation, differentiating agents promote the process by which cells acquire the specialized structural and functional traits of differentiated cells.

When cells undergo differentiation, they also lose the capacity to divide. Agents that promote cell differentiation therefore tend to decrease the overall level of cell proliferation. An example of a differentiating agent used in cancer therapy is retinoic acid, a form of vitamin A employed in the treatment of acute promyelocytic leukemia.

13. Essay on Cancer Treatment: (Around 850 Words)

Toxic Side Effects and Drug Resistance Limits the Effectiveness of Chemotherapy :

The ultimate goal of chemotherapy is to destroy or restrain the proliferation of cancer cells without harming normal cells. However, with the exception of hormones and differentiating agents, which are useful for only a few selected types of cancer, most chemotherapeutic drugs act by inhibiting DNA replication, damaging DNA, or blocking cell division—actions that are detrimental to normal dividing cells as well as to cancer cells.

Moreover, because chemotherapeutic drugs circulate throughout the body, they encounter normal dividing cells no matter where the cells reside. For example, the hair loss that commonly accompanies chemotherapy is a toxic side effect that is triggered when circulating drugs encounter the dividing cells that line the hair follicles.

The most serious side effects of chemotherapy involve the gastrointestinal tract and the bone marrow. As with radiation therapy, damage to normal dividing cells in these tissues can lead to nausea, vomiting, diarrhea, anemia, defective blood clotting, and immune deficiency.

Such side effects usually tend to be more severe with chemotherapy than with radiation because drugs cannot be easily focused on a particular region of the body to minimize toxicity to the gastrointestinal tract and bone marrow.

Fortunately, some cancer cells are particularly sensitive to chemotherapy and can be destroyed without excessive toxicity to normal cells; for many cancers, however, chemotherapy may fail because the drug dosage required to kill all cancer cells would trigger overwhelmingly toxic side effects.

Another problem that can reduce the effectiveness of chemotherapy is the tendency for tumors to become resistant to the killing effects of anticancer drugs, especially after a prolonged series of treatments. Even if most of the cancer cells in a person’s body are destroyed by a particular drug, a few drug-resistant cells present in the initial population could proliferate and form a new tumor that would then be completely resistant to the drug.

And if drug-resistant cells are initially absent, cancers tend to be genetically unstable and may acquire mutations that impart drug resistance during the course of treatment. An illustration of this problem is provided by methotrexate, an anticancer drug that inhibits the enzyme dihydrofolate reductase (see Figure 8).

In cancers that are being treated with methotrexate, the gene for dihydrofolate reductase sometimes undergoes mutation or amplification. The mutations create altered forms of dihydrofolate reductase that are no longer inhibited by methotrexate, and gene amplification leads to increased production of dihydrofolate reductase, thereby diminishing the effectiveness of methotrexate treatment. Such genetic changes, which alter the target of a drug to make it less susceptible to the drug’s effects, are commonly observed in individuals receiving chemotherapy.

Given the large number of anticancer drugs available, it might seem that a simple solution would be to just switch drugs when resistance arises. Unfortunately, the situation is complicated by the fact that tumors often develop resistance to several drugs at the same time, even though only a single drug is administered.

One way in which cancer cells become resistant to multiple drugs is by producing plasma membrane proteins that actively pump drugs out of the cells. These drug-pumping proteins, called multidrug resistance transport proteins, have a remarkably broad specificity. They export a wide range of chemically dissimilar molecules, thereby imparting resistance to a broad spectrum of drugs.

Another factor that can contribute to multidrug resistance is related to the mechanism by which anticancer drugs kill cells. Although multiple killing mechanisms appear to be involved, chemotherapeutic drugs sometime act by damaging DNA to such an extent that apoptosis is invoked to destroy the damaged cell.

In such cases, the effectiveness of chemotherapy may be reduced by mutations that disable apoptosis. Mutations of this type are often present at the time of initial diagnosis, or they may arise during chemotherapy. In either case, mutations that disable apoptosis would be expected to decrease the effectiveness of any drug that kills a particular type of cancer cell primarily by triggering apoptosis.

Another possible source of drug resistance is related to the heterogeneity of tumor cell populations. A growing body of evidence suggests that in any given tumor, only a small population of cells, called cancer stem cells, are able to proliferate indefinitely.

The existence of these cancer stem cells, which have been postulated to give rise to all the other cells found in a tumor, could help explain why treatments that cause tumors to shrink until they are undetectable may still not cure the disease.

While the treatment may eliminate the bulk of the cancer cells, a few remaining cancer stem cells may be all that is needed to replenish the tumor cell population. According to this theory, existing anticancer drugs may be more effective at killing the majority of a person’s tumor cells than they are at killing the rare cancer stem cells, which then regenerate the tumor after treatment is stopped.

Researchers are currently exploring this idea by searching for cancer stem cells in various tumor types and testing to see whether they exhibit any unique properties that could be targeted by future anticancer drugs.

14. Essay on Cancer Treatment: (Around 700 Words)

Combination Chemotherapy and Stem Cell Transplants are Two Strategies for Improving the Effectiveness of Chemotherapy :

For certain kinds of cancer, chemotherapy is successful in restoring normal life expectancies to many patients. Sometimes the chemotherapy by itself is responsible for the improved prognosis, but it is more common for chemotherapy to be used in conjunction with surgery or radiation.

Despite these successes, the effectiveness of chemotherapy is often hindered by the emergence of drug resistance and by the toxic side effects that restrict the dose that can be safely administered.

Additional challenges are raised by the need for delivery techniques that convey drugs to tumor sites at the proper concentration for an appropriate period of time and by the existence of heterogeneous tumor populations containing mixtures of cells that respond differently to the same drug.

One strategy for trying to improve the effectiveness of chemotherapy is to administer several drugs in combination rather than a single agent alone. Drug combinations are often named using an acronym that is derived from the initials of the drugs being used. For example, BEP chemotherapy (bleomycin, etoposide, and Platinol) is the name of a treatment for testicular cancer, and CMF chemotherapy (cyclophosphamide, methotrexate, and fluorouracil) is the name of a treatment for breast cancer.

This general approach, known as combination chemotherapy, is most effective with drugs that differ in their mechanisms of action. For example, consider three drugs exhibiting different side effects that limit the dose of each that can be safely administered. Combining the three drugs at their maximum tolerated doses will increase the overall tumor-killing effectiveness compared with each drug by itself, and yet the overall toxicity may remain at an acceptable level because each drug works in a different way.

Another advantage of drug combinations is that cancer cells are less likely to become resistant to chemotherapy when several drugs are administered simultaneously, especially if the drugs differ in their chemical properties, cellular targets, and mechanisms of action. The enormous challenge of combination therapy is finding the most effective drug mixtures for each type of cancer, especially given the dozens of drugs that could in theory be administered in thousands of different combinations.

Another approach for improving the effectiveness of chemotherapy deals with the potential problem of bone marrow damage. Many anticancer drugs are capable of killing all cancer cells if the dose is raised high enough. The dose that can be realistically administered, however, is limited by toxicity to the bone marrow, which contains the hematopoietic stem cells whose proliferation gives rise to blood cells.

If too many of these stem cells are destroyed during high-dose chemotherapy, blood cells will not be produced and a person cannot survive. One approach for addressing this problem is to use high-dose chemotherapy to destroy all cancer cells and then follow the treatment with stem cell transplantation (also called bone marrow transplantation) to replenish the person’s hematopoietic stem cells. Under such conditions, higher drug doses can be used because the blood-forming stem cells destroyed by the chemotherapy are subsequently being replaced.

The stem cells used for transplantation can be obtained either from a cancer patient’s own bone marrow or blood prior to administration of high-dose chemotherapy, or from the bone marrow or blood of a genetically compatible individual who is willing to serve as a stem cell donor.

Unfortunately, each approach has its complications. Using a cancer patient’s own stem cells for subsequent transplantation creates the risk of either reintroducing cancer cells or relying on stem cells that have been damaged during earlier cancer treatments. On the other hand, finding an appropriately matched donor can be difficult, and immune cells present in the donor’s blood or bone marrow sometimes attack the tissues of the cancer patient, thereby creating a potentially life-threatening condition known as graft-versus-host disease.

An alternative is to use umbilical cord blood rather than bone marrow or peripheral blood as a source of stem cells for transplantation. The umbilical cord, which is normally discarded at birth, contains blood with a large number of hematopoietic stem cells.

These cells elicit a lower incidence of graft-versus-host disease, do not require as close a genetic match as do adult stem cells, and are readily obtained from blood banks that store frozen umbilical cord blood taken from healthy newborns. The possible usefulness of cord blood as a source of stem cells for cancer patients is currently under investigation.

15. Essay on Cancer Treatment: (Around 600 Words)

Molecular and Genetic Testing is Beginning to Allow Cancer Treatments to be Tailored to Individual Patients :

A final approach for enhancing the effectiveness of chemotherapy involves the possibility of designing drug treatments that are personalized for each individual patient. It has been known for many years that cancer patients with tumors that are indistinguishable from one another by traditional criteria often exhibit different outcomes after receiving the same treatment.

Experiments using DNA microarray technology to analyze gene activity have provided a likely explanation: Cancers of the same type exhibit different patterns of gene expression that cause them to behave differently. The Oncotype DX gene expression test, which measures the activity of 21 key genes in breast cancer cells, is able to predict which patients are most likely to have their cancers recur after surgery.

In the absence of such information, doctors would usually recommend that most patients receive chemotherapy. The value of gene expression testing is that it can help identify those patients who really need chemotherapy and are likely to benefit from it.

Taking this approach one step further, analyzing cancer specimens for gene expression patterns and the presence of specific mutations may provide information about the exact type of cancer treatment that is most appropriate for each person. A striking example is provided by Iressa.

Iressa, which acts by inhibiting the receptor for epidermal growth factor (EGF), has been approved for use in the treatment of lung cancer. Tumor shrinkage occurs in only about 10% of the patients treated with Iressa, but when the drug does work, it works extremely well.

The reason Iressa is more effective in some individuals than others has been traced to the presence of a mutant form of the EGF receptor gene in the cancers of those patients who respond well to the drug.

When lung cancer cells containing the mutant form of the EGF receptor are grown in laboratory culture, they are found to be much more sensitive to the growth-inhibiting effects of Iressa than are cancer cells that contain the normal form of the EGF receptor (Figure 12).

This discovery opens the door to a personalized type of cancer therapy in which genetic testing of cancer cells is used to identify those particular patients who are most likely to benefit from treatment with Iressa.

A patient’s hereditary background can also affect how he or she responds to different types of treatment. For example, inherited genes that influence steps in drug metabolism have been found to influence how well a person responds to different kinds of drugs. It is therefore hoped that a better understanding of patient-specific and tumor-specific differences in genetic makeup will eventually allow treatments to be tailor-made for each individual cancer patient.

The use of surgery, radiation, or chemotherapy—either alone or in various combinations—can cure or significantly prolong survival times for many types of cancer, especially when the disease is diagnosed early. However, some of the more aggressive cancers, including those involving the lung, pancreas, or liver, are difficult to control in these ways, nor are current approaches very successful with cancers diagnosed in their advanced stages.

In trying to find more effective ways of treating such cancers, scientists have been working to develop “magic bullets” that will selectively seek out and destroy cancer cells without damaging normal cells in the process. Although this goal presents a formidable challenge, several approaches for achieving better selectivity in targeting cancer cells are beginning to show signs of success.

Essay # 16. Essay on Cancer Treatment: (Around 400 Words)

Immunotherapies Exploit the Ability of the Immune System to Recognize Cancer Cells :

One way of introducing better selectivity into cancer treatments is to exploit the ability of the immune system to recognize cancer cells. This general approach, called immunotherapy, was first proposed in the 1800s after doctors noticed that tumors occasionally regress in people who develop bacterial infections.

Since infections stimulate the immune system, it was postulated that the stimulated immune cells might be attacking cancer cells as well as the invading bacteria. Efforts were therefore made to build on this idea by using live or dead bacteria to provoke the immune system of cancer patients. Some success was eventually seen with Bacillus Calmette- Guerin (BCG), a bacterial strain that does not cause disease but elicits a strong immune response at the site where it is introduced into the body.

One use of BCG is in the treatment of early stage bladder cancers that are localized to the bladder wall. After the cancer is surgically removed, inserting BCG into the bladder elicits a prolonged activation of immune cells that leads to lower rates of cancer recurrence.

Although this example demonstrates the potential value of stimulating the immune system, BCG must be administered directly into the bladder to provoke an immune response at the primary tumor site.

With other types of cancer, especially when they have metastasized to unknown locations, it becomes necessary to stimulate an immune response against cancer cells wherever they may have traveled. For this purpose scientists have turned to molecules called cytokines, which are proteins produced by the body to stimulate immune responses against infectious agents.

The first cytokine found to be helpful in treating cancer was interferon alpha, a protein produced in response to viral infections. Interferon alpha is used in the treatment of several kinds of cancer, including hairy cell leukemia and Kaposi’s sarcoma. Interleukin-2 (IL-2) and tumor necrosis factor (TNF) are two other cytokines that are being evaluated for possible use as immune stimulators in cancer patients.

IL-2 and TNF both elicit a strong antitumor response in laboratory animals, but they are extremely toxic when administered to humans. At present, TNF is still under active investigation and IL-2 is an approved treatment for advanced kidney cancer and melanoma.

As we will see shortly, IL-2 is also being used experimentally to stimulate antitumor lymphocytes that are isolated from a patient’s tumor site and grown in the laboratory prior to being injected back into the bloodstream.

17. Essay on Cancer Treatment: (Around 400 Words)

Large Quantities of Identical Antibody Molecules can be Produced Using the Monoclonal Antibody Technique :

BCG and cytokines are relatively nonspecific approaches to immunotherapy because they strengthen the overall activity of the immune system rather than preferentially directing an attack against cancer cells. Devising immunotherapies that act more selectively requires approaches for distinguishing cancer cells from normal cells.

The immune system sometimes recognizes cancer cells through the presence of specific antigens that cancer cells carry. One way in which the immune system responds to antigens is by producing antibodies, which are soluble proteins manufactured by immune cells known as B lymphocytes. Antibodies circulate in the bloodstream and penetrate into extracellular fluids, where they specifically bind to the antigens that triggered the immune response.

Antibody molecules recognize and bind to their corresponding antigens with extraordinary precision, making antibodies ideally suited to serving as “magic bullets” that selectively target antigens that are unique to (or preferentially concentrated in) cancer cells.

For many years, the use of antibodies for treating cancer was hampered by the lack of a reproducible method for producing large quantities of pure antibody molecules directed against the same antigen. Then in 1975, Georges Kohler and Cesar Milstein solved the problem by devising the procedure illustrated in Figure 13.

In this technique, animals are injected with material containing an antigen of interest, and antibody-producing lymphocytes are isolated from the animal a few weeks later. Within such a heterogeneous lymphocyte population, each lymphocyte produces a single type of antibody directed against one particular antigen.

To facilitate the selection and growth of individual lymphocytes, the lymphocytes are fused with cells that divide rapidly and have an unlimited lifespan in culture. The resulting hybrid cells are then individually selected and grown to form a series of clones called hybridomas.

The antibodies produced by hybridomas are referred to as monoclonal antibodies because each one is a pure antibody produced by a cloned population of lymphocytes. Hybridomas can be maintained in culture indefinitely and represent inexhaustible sources of individual antibody molecules, each directed against a different antigen.

18. Essay on Cancer Treatment: (Around 600 Words)

Monoclonal Antibodies can be Used to Trigger Cancer Cell Destruction Either by themselves or Linked to Radioactive Substances :

The ability to obtain monoclonal antibodies in large quantities gave rise to high expectations regarding their usefulness for selectively targeting cancer cells. The basic strategy is to immunize animals with human cancer tissue and then select those monoclonal antibodies that bind to antigens on the cancer cell surface.

When they are injected into individuals with cancer, these antibody molecules would be expected to circulate throughout the body until they encounter cancer cells. The antibodies then bind to the cancer cell surface, where their presence triggers an immune attack that destroys only those cells to which the antibody is attached (Figure 14, top).

Antibodies can also be used as delivery vehicles for toxic molecules by linking them to radioactive substances, chemotherapeutic drugs, or other kinds of toxic substances that are too lethal to administer alone (Figure 14, bottom).

Attaching these substances to monoclonal antibodies allows the toxins or radioactivity to be selectively concentrated at tumor sites by the antibody without accumulating to toxic levels elsewhere in the body.

Although this strategy sounds simple in theory, several obstacles have slowed its application to cancer patients. One problem is that monoclonal antibodies are usually produced in mice by injecting them with human cancer tissue.

The resulting antibodies are therefore recognized as foreign proteins when administered to cancer patients, who mount an immune response that inactivates the mouse antibody molecules, especially if the antibody is administered more than once.

For this reason, monoclonal antibodies cannot be used for repeated treatments unless they are first made more human-like by replacing large parts of the mouse antibody molecule with corresponding sequences derived from human antibodies.

A second complication encountered with monoclonal antibodies is that the cancer cell antigens they recognize may be present on certain normal cells as well. Each newly developed antibody must therefore be tested by linking it to a radioisotope and injecting it into patients to see whether the radioactivity becomes preferentially localized to sites where tumor cells are present.

The preceding issues have complicated the development of antibody-based therapies, but several successes have already been achieved. For example, the monoclonal antibodies Rituxan, Zevalin, and Bexxar are now among the approved treatments for non-Hodgkin’s B cell lymphoma.

All three antibodies target B lymphocytes for destruction by binding to the CD20 antigen, which is present on the surface of malignant as well as normal B lymphocytes. Although antibodies that target CD20 are toxic to normal B lymphocytes, CD20 is not present on the precursor cells whose proliferation gives rise to B lymphocytes.

These precursor cells therefore replenish the normal B lymphocyte population that is inadvertently destroyed along with malignant B lymphocytes during antibody treatment (Figure 15).

Besides being administered by themselves, monoclonal antibodies directed against CD20 have been linked to radioactive chemicals and used to direct high doses of radiation to tumor sites, which may be more effective in killing cancer cells than the use of antibodies alone. Radioactive antibodies are also useful for determining where cancer cells are localized and for monitoring changes in tumor cell numbers in response to treatment.

The value of monoclonal antibodies is not restricted to their ability to target cancer cells for destruction. Monoclonal antibodies have also been developed that target signaling pathway components required by cancer cells for their proliferation.

For example, some breast cancer patients are being treated with Herceptin, a monoclonal antibody that binds to and blocks a growth factor receptor. Because monoclonal antibodies are not the only tools used for targeting signaling pathway components, we will delay a discussion of this type of cancer therapy until the section on molecular targeting.

19. Essay on Cancer Treatment: (Around 450 Words)

Several Types of Cancer Vaccines are Currently under Development :

Antibodies are one of two basic mechanisms used by the immune system for attacking foreign antigens. The second mechanism, known as cell-mediated immunity, utilizes cytotoxic T lymphocytes that bind to the surface of cells exhibiting foreign antigens and kill the targeted cells by causing them to burst. This tactic is normally used to destroy cells harboring infectious agents such as viruses, bacteria, and fungi, and it also plays a role in the destruction of foreign tissue grafts and organ transplants.

The realization that cytotoxic T lymphocytes might be able to mount an attack against cancer cells first emerged in the 1940s from studies in which cancer was induced in mice by exposing them to carcinogenic chemicals or viruses. The resulting tumors were found to contain antigens whose administration to other mice immunized the animals against transplants of the same tumor.

When T lymphocytes were isolated from the immunized animals, these T lymphocytes could kill tumor cells in culture and transfer tumor immunity when injected into other animals. In contrast, antibodies produced by the tumor-bearing animals were relatively ineffective at killing cancer cells or transferring immunity.

These observations have stimulated interest in the idea of developing vaccines that will stimulate a cancer patient’s own T lymphocytes to attack cancer cells. The underlying rationale is that tumor antigens tend to be weak antigens that do not elicit a strong immune response, but an appropriate vaccine might be able to present the antigens in a way that would stimulate the immune system to become more aware of their existence.

Among the candidates for vaccine antigens are the abnormal proteins that cancer cells produce as a result of genetic mutations. Since these proteins are not produced by normal cells, putting them into vaccines should stimulate an immune response that is selectively directed against cancer cells. Other proteins that are overproduced by tumors might also be useful candidates for incorporation into cancer vaccines.

It is possible to vaccinate cancer patients by simply injecting them with tumor antigens, but attempts are being made to improve vaccination efficiency by first introducing the antigens into dendritic cells for antigen processing. Triggering an efficient immune response requires that antigens be broken into fragments and presented to the immune system by antigen-presenting cells such as dendritic cells.

When dendritic cells obtained from cancer patients are grown in the laboratory together with tumor antigens, the dendritic cells take up the antigens, chop them into pieces, and present the resulting fragments on their cell surface in a way that activates an immune response. Experiments are currently under way to determine whether the injection of such antigen-loaded dendritic cells into patients is a feasible tactic for treating cancer.

20. Essay on Cancer Treatment: (Around 500 Words)

Adoptive-Cell-Transfer Therapy Uses a Person’s own Antitumor Lymphocytes that have been Selected and Grown in the Laboratory :

Adoptive-cell-transfer (ACT) therapy is an alternative to vaccination in which a patient’s own lymphocytes are first isolated, selected, and grown in the laboratory to enhance their cancer-fighting properties prior to injecting the cells back into the body. The underlying reasoning is that individuals with cancer often possess lymphocytes that are capable of attacking tumor cells, but these lymphocytes are not produced in sufficient quantities to keep the tumor under control.

ACT therapy attempts to solve this problem by removing some of these lymphocytes from the body and increasing their numbers by growing them in culture prior to reintroducing the cells into the patient.

If a person with cancer has any lymphocytes that are capable of attacking tumor cells, the most likely place to find them would be within the tumor itself. Lymphocytes that are located at the tumor site, called tumor-infiltrating lymphocytes (TILs), have therefore been used as a source of cells for ACT therapy.

In one set of studies, illustrated in Figure 16, multiple samples of TILs were isolated from the tumors of advanced stage melanoma patients and tested for their ability to attack tumor cells. TIL samples exhibiting the greatest anti-tumor activity were then selected and grown in culture in the presence of interleukin-2 (IL-2), a cytokine that stimulates the proliferation and cancer-destroying properties of the lymphocytes.

Before introducing the tumor-killing lymphocytes back into the body, each cancer patient was treated with high-dose chemotherapy to destroy a large fraction of their existing lymphocytes.

The tumor-killing lymphocytes were then injected back into the bloodstream and the patients were treated with IL-2 to further stimulate the proliferation of the injected cells. The net result was that tumor-killing lymphocytes became a large portion of each person’s immune system, and a significant number of patients experienced tumor regressions.

ACT therapy is still an experimental procedure and will be difficult to apply to large numbers of patients, but these results suggest that cancer therapies may eventually be able to exploit the ability of lymphocytes to recognize and kill cancer cells. Several problems remain to be solved, however.

First, the possibility exists that lymphocytes targeted against cancer cell antigens will mistakenly attack healthy cells possessing similar antigens. Another problem is that cancer cells can devise ways of evading immune attack. For example, sometimes cancer cells acquire mutations that cause them to stop making the antigens being targeted by the immune system.

In other cases, cancer cells become resistant to immune attack by producing molecules that either kill lymphocytes or disrupt their ability to function. Of course, the possibility that resistance will develop is not unique to immunotherapy; we have already seen that resistance arises with chemotherapy as well. For this reason, a combination of different therapeutic approaches may end up being the best approach for treating cancer.

21. Essay on Cancer Treatment: (Around 500 Words)

Herceptin and Gleevec are Anticancer Drugs that Illustrate the Concept of Molecular Targeting :

Until the early 1980s, research into new cancer treatments focused largely on the development of drugs that disrupt DNA synthesis and interfere with cell division. Although some of the resulting drugs have turned out to be useful in treating cancer, their effectiveness is often limited by toxic effects on normal dividing cells.

In the past two decades, the identification of specific genes whose mutation or altered expression can lead to cancer has opened up a new possibility—molecular targeting—in which drugs are designed to target those proteins that are critical to the cancerous state.

One way to pursue the goal of molecular targeting is to take advantage of the specificity of antibodies. Substantial efforts are currently being made to develop monoclonal antibodies that bind to and inactivate key proteins involved in the signaling pathways required for cancer cell proliferation.

The first such antibody to be approved for use in treating cancer patients, called Herceptin, binds to and inactivates a cell surface growth factor receptor called the ErbB2 receptor, which is produced by the ERBB2 gene (also called HER2).

About 25% of all breast and ovarian cancers have amplified ERBB2 genes, which produce excessive amounts of ErbB2 receptor that in turn causes hyperactive signaling. When individuals whose cancers overexpress the ErbB2 receptor are treated with Herceptin, the Herceptin antibody binds to the ErbB2 receptor and the ability of the receptor to stimulate cell proliferation is blocked, thereby slowing or stopping tumor growth.

Monoclonal antibodies are not the only way to target specific molecules for inactivation. Another approach, called rational drug design, involves the laboratory synthesis of small molecule inhibitors that are designed to bind to and inactivate specific target molecules. Unlike antibodies, these inhibitors are small enough to enter cells and affect intracellular proteins.

One of the first such drugs to be developed, called Gleevec (generic name – imatinib), is a small molecule that binds to and inhibits the abnormal tyrosine kinase produced by the BCR-ABL oncogene present in chronic myelogenous leukemias. BCR-ABL is a fusion gene generated during the chromosomal translocation that creates the Philadelphia chromosome.

Because it arises from the fusion of DNA sequences derived from two different genes, BCR-ABL produces a structurally abnormal protein—the Bcr-Abl tyrosine kinase—that represents an ideal drug target because it is produced only by cancer cells.

Initial studies of the effectiveness of Gleevec as a treatment for chronic myelogenous leukemia were extremely encouraging, In patients with early stage disease, more than 50% had no signs of cancer six months after treatment (a response rate ten times better than had been seen before).

Unfortunately, patients with late stage disease frequently develop mutations that alter the structure of the Bcr-Abl tyrosine Kinase, thereby making it resistant to Gleevec. Additional small molecule inhibitors that overcome this resistance to Gleevec have been developed, but it takes many years to take each new compound through the necessary testing before it can be approved for routine medical use.

22. Essay on Cancer Treatment: (Around 800 Words)

A Diverse Group of Potential Targets for Anticancer Drugs are Currently being Investigated :

The drugs Herceptin and Gleevec illustrate two different approaches—monoclonal antibodies and small molecule inhibitors—for targeting specific proteins found in cancer cells. These two drugs are relatively recent accomplishments in the long history of cancer drug research; Herceptin was introduced in 1998 and Gleevec in 2001.

As might be expected, their success has stimulated interest in developing other drugs that target molecules important to cancer cells. For example, the introduction of Gleevec in 2001 was followed in 2003 by another small molecule inhibitor called Iressa (generic name gefitinib).

Iressa targets the receptor for epidermal growth factor and is effective in a subset of lung cancer patients whose cancer cells possess a mutant form of the EGF receptor (see Figure 12).

Dozens of other drugs based on the principle of molecular targeting are currently under investigation. Tyrosine kinases and growth factor receptors (the targets for Gleevec and Herceptin, respectively) are just two of many potential targets. The uncontrolled proliferation of cancer cells can be traced to disruptions in a variety of growth signaling pathways, including the Ras-MAFK, JaK-STAT, Wnt, and PI3K-Akt pathways.

Any of the proteins involved in these pathways could represent a potential target for an anticancer drug. Other proteins whose activities contribute to the six hallmark traits of cancer cells might likewise be good candidates. Table 3 lists some examples of proteins in these various categories that are now being investigated as potential targets for anticancer drugs.

Despite the attractiveness of molecular targeting, many of the drugs developed after the initial successes with Herceptin and Gleevec have failed to work well when tested in cancer patients. While such disappointments may simply mean that these particular drugs are ineffective, several factors complicate the testing of anticancer drugs that could have contributed to the failures.

First, targeted therapies would only be expected to work in those individuals whose cancer cells exhibit the appropriate molecular target. Since cancers of the same type often differ in their molecular properties from person to person, obtaining a molecular profile of each person’s tumor might assist in identifying patients most likely to benefit from a given type of treatment.

Second, testing of new drugs is generally done in patients who also receive standard chemotherapy, which might obscure the benefits of an experimental drug. For example, in the case of tamoxifen, which targets the estrogen receptor, inferior results are obtained when tamoxifen is combined with standard chemotherapy compared with giving tamoxifen either alone or after chemotherapy.

In theory, the most reliable results would be obtained by comparing a new drug given to one group of patients versus standard chemotherapy given to another group of patients. However, ethical considerations make it inappropriate to withhold standard treatment from the first group of patients if the standard treatment is known to be beneficial.

A third type of problem is related to the need for better drug delivery methods that reliably convey drugs to tumor sites at the proper concentration for an appropriate period of time. In many cases, drugs are simply degraded too quickly after entering the body and do not accumulate in tumor tissues.

One way to improve drug delivery is through the use of water-soluble polymers such as polyethylene glycol or N-(2-hydroxypropyl) methacrylamide. Binding drugs to these polymers prolongs a drug’s lifetime in the body and alters its pattern of distribution.

The reason for the altered behavior is that the large size of drug-polymer complexes prevents them from passing out of the bloodstream and into cells as rapidly as the free drug itself. In addition, tumor blood vessels tend to be “leaky,” causing drug-polymer complexes to leave the bloodstream and enter tumor tissues more readily than normal tissues.

A final problem that complicates drug testing is that clinical trials are usually carried out in late-stage cancer patients after all other treatments have failed. At this advanced stage, targeted molecular therapy may no longer be useful. For example, consider the behavior of drugs that inhibit matrix metalloproteinases (MMPs), which are attractive targets because they play important roles in angiogenesis, tissue invasion, and metastasis.

Animal studies have shown that MMP inhibitors are effective antitumor agents during the early stages of cancer progression, when tumor invasion and metastasis are just beginning. Human testing, however, has been performed mainly in patients with late stage disease, when MMP inhibitors appear to be largely ineffective.

This is just one of many examples of experimental anticancer drugs that have been tested in late stages of cancer progression rather than early in the disease, when they are more likely to work. Such problems are difficult to avoid for the simple reason that experimental new treatments are not likely to be tried on patients until other treatments have failed, at which point the disease may have reached an advanced stage that makes it unresponsive to targeted therapies.

23. Essay on Cancer Treatment: (Around 600 Words)

Anti-Angiogenic Therapy Illustrates the Difficulties Involved in Translating Laboratory Research into Human Cancer Treatments:

Tumor growth and metastasis depend on angiogenesis— that is, the growth of blood vessels that supply nutrients and oxygen to tumor cells and remove waste products. It is therefore logical to expect that angiogenesis inhibitors might be useful for treating cancer patients.

Initial support for this concept of anti-angiogenic therapy came from the studies of Judah Folkman, who reported that treating tumor-bearing mice with the angiogenesis- inhibiting proteins angiostatin and endostatin makes tumors shrink and disappear. When these experiments were first described in 1998 in a front page story appearing in the New York Times, a distinguished scientist was quoted as saying, “judah is going to cure cancer in two years.”

Needless to say, such sensational news coverage led to unrealistic expectations concerning the prospects for an immediate cancer cure. Applying the results of animal studies to human patients takes many years of testing, and humans do not always respond in the same way as animals.

Dozens of angiogenesis-inhibiting drugs are therefore being evaluated in cancer patients to see if the promising results observed in animals will apply to humans. On the positive side, the early human studies showed that anti-angiogenic therapy elicits few of the harsh side effects seen with chemotherapy, and in a few cancer patients, tumors seemed to stop growing. However, some disappointment was expressed with the early results because they failed to show the quick cure for cancer that people had been led to expect.

Of course, expectations for a quick cancer cure were unrealistic, and there are many reasons why it would be premature to come to any definitive conclusions at this point regarding the effectiveness of anti-angiogenic therapy. First, the early human trials were carried out mainly on cancer patients with late stage disease, and anti-angiogenic therapy may work better at earlier stages.

Second, the optimal dose for angiogenesis-inhibiting drugs may need to be tailored to each individual patient based on the concentration of angiogenesis-stimulating molecules their tumors produce. Third, angiogenesis inhibitors may work best when their concentration within the body is maintained at a relatively constant level, which is quite different from the way in which standard chemotherapy is typically, administered using large intermittent doses.

Finally, the effectiveness of anticancer drugs is usually measured by assessing their ability to make tumors shrink or disappear. This outcome might be an appropriate expectation for a drug that kills cancer cells, but inhibiting blood vessel growth may simply stop tumors from becoming any larger.

Such a state, called stable disease, could represent an acceptable outcome for an anti-angiogenic drug if it allowed patients to live with cancer as a chronic but manageable disease condition, especially in view of the minimal side effects associated with the use of angiogenesis inhibitors.

The complexities raised by the preceding issues mean that it will take many years to assess the effectiveness of angiogenesis-inhibiting drugs and determine how best to use them. Nonetheless, signs of progress are already evident. In 2004, Avastin became the first anti-angiogenic drug to be approved for routine medical use in cancer patients.

Avastin is a monoclonal antibody that binds to and inactivates the angiogenesis-stimulating growth factor, VEGF. In tumors that depend on VEGF to stimulate angiogenesis, blocking VEGF with Avastin would be expected to inhibit angiogenesis and thereby inhibit tumor growth.

Human clinical trials have shown that patients with metastatic colon cancer who received standard chemotherapy plus Avastin lived longer than patients who received standard chemotherapy without Avastin. These results were one of the first signs that anti-angiogenic therapy may one day become an integral component of human cancer treatment.

24. Essay on Cancer Treatment: (Around 900 Words)

Engineered Viruses are Potential Tools for Repairing or Killing Cancer Cells :

Over the past two decades, the roles played by oncogenes and tumor suppressor genes in the development of cancer have become increasingly apparent. This discovery raises the possibility of attacking the disease at its root cause- defective genes. In other words, rather than trying to kill or restrain the proliferation of cancer cells, it might be possible to repair the defective genes that are responsible for the cancerous state.

The process of replacing defective genes with normal versions is called gene therapy. Gene therapy was initially envisioned as a treatment for genetic diseases in which a person inherits a single defective gene, such as a gene responsible for cystic fibrosis, hemophilia, or certain immune deficiencies.

Curing illnesses of this type would simply require that a normal copy of the single defective gene be inserted into a person’s cells under conditions that allow the inserted gene to be actively expressed.

While the concept sounds simple in theory, it is difficult to transfer genes into cells efficiently under conditions that permit the transferred genes to become permanently incorporated and expressed. As a result, gene therapy had been of limited usefulness in treating genetic diseases thus far.

Applying gene therapy to cancer is even more complicated than treating an inherited genetic disease because it may be necessary to repair the defect in all cancer cells, not just some of them. Moreover, cancer cells usually exhibit defects in several genes rather than just one, although it may not be necessary to repair them all. Human cancers often exhibit defects in the p53 pathway that prevent cells from undergoing apoptosis.

If this single pathway could be restored, the other abnormalities exhibited by cancer cells might trigger the p53 pathway and cause the cells to self-destruct by apoptosis. Attempts have therefore been made to repair the p53 gene in cancers in which this gene is defective (Figure 17).

Support for this approach has come from animal studies showing that tumor regression can be induced by injecting animals with a virus whose DNA contains a normal copy of the p53 gene. In early human testing, a similar virus injected into the tumors of lung cancer patients has been found to restore p53 production and induce disease stabilization in some patients.

An alternative to using viruses for gene therapy is to engineer them to kill cancer cells selectively. It has been known for many years that some viruses cause infected cells to rupture and die, a process called lysis. Attempts are therefore being made to create viruses that selectively infect and cause the lysis of cancer cells.

One of the first of these viruses to be tested in humans was ONYX-O15, an adenovirus containing a mutation designed to permit the virus to replicate only in cells with a defective p53 pathway.

Since the p53 pathway is defective in a majority of human cancers, it was predicted that ONYX-015 might be a broadly useful tool for killing cancer cells. Early investigations appeared to verify the ability of ONYX-015 to replicate preferentially in cancer cells, but follow-up studies failed to confirm the dependence of viral replication on the presence of a defective p53 pathway and future development of this particular virus is uncertain.

ONYX-015, however, represents just one of many engineered viruses that are being developed to kill cancer cells without harming normal cells. Like ONYX-015, these viruses have been genetically altered to make their replication dependent either on the absence of genes that are inactive only in cancer cells or on the presence of genes that are active only in cancer cells (Figure 18, left).

Another potential strategy is to modify viruses in ways that cause them to interact preferentially with cancer cells, perhaps by altering viral coat proteins so that they bind to receptors present on the surface of cancer cells (see Figure 18, right). Such approaches are currently under active investigation to see whether they might be of any use in the treatment of cancer.

Before any new treatment can be incorporated into standard medical practice, it must first undergo a lengthy and painstaking evaluation process. In the early days of cancer research, identifying and evaluating new treatments was especially time consuming because anticancer drugs were often discovered through a largely random approach.

For example, the National Cancer Institute established a massive screening program in the mid-1960s that systematically tested thousands of chemical compounds for possible anticancer activity. Those substances that exhibited the most promise in killing cancer cells in laboratory culture or in animal studies were eventually tested in humans, and a number of drugs now used in cancer chemotherapy were discovered in this way.

In recent years, our growing understanding of the molecular abnormalities exhibited by cancer cells has permitted more selective approaches for developing drugs that target cancer cells. Nonetheless, such drugs still require extensive testing before they can be incorporated into standard medical practice.

The testing process, which is regulated in the United States by the Food and Drug Administration (FDA), requires that any drug proposed for human use first undergo preclinical testing in animals to demonstrate that the treatment is safe and effective.

If successful, animal testing is followed by an extensive series of human tests to determine whether the drug works in humans and whether it compares favorably to existing methods of treatment.

25. Essay on Cancer Treatment: (Around 650 Words)

Human Clinical Trials Involve Multiple Phases of Testing :

Evaluating a new drug in humans involves a series of tests called clinical trials. Patients who volunteer for a clinical trial are given information regarding the nature of their disease, the potential risks and benefits of the treatment being tested, and the availability of other treatment options.

Before participating, all patients must sign informed consent documents indicating their understanding of these conditions and providing their voluntary consent. Each trial involves several phases of testing; often requiring five to ten years to complete at a cost of several hundred million dollars, before a drug can be approved for routine medical use (Figure 19).

In the first phase of testing, called a Phase I clinical trial, a new drug is administered to several dozen people to determine the safe dose. The first few individuals are given a very low dose of the drug and monitored closely for toxic side effects. If the drug is well tolerated, the dose is gradually increased in subsequent groups of patients until an appropriate dose is determined that is likely to be effective without severe side effects.

If the drug is found to be reasonably safe, the optimal dose determined during Phase I testing is then administered to a somewhat larger group of cancer patients—usually from 25 to 100—in a Phase II clinical trial to determine whether the drug exhibits any effectiveness in treating cancer. Evidence of effectiveness might be the complete disappearance of a tumor (complete response), a tumor that gets smaller (partial response), or a tumor that stops growing (stable disease). To justify further testing, a significant percentage of the treated patients must exhibit one of these three responses.

The required percentage may vary, however, depending on the type of cancer being treated and the effectiveness of currently available drugs. For example, a 10% response rate might justify continued testing of a treatment for an aggressive tumor like pancreatic cancer that tends to be resistant to most current drugs, whereas a much higher response rate would be required for low-grade lymphomas, for which several effective drugs are already available.

If a drug exhibits sufficient signs of anticancer activity in Phase II testing, its effectiveness and safety are thoroughly evaluated in a Phase III clinical trial. A Phase III trial is a randomized trial in which hundreds or thousands of patients are randomly assigned to two different groups- an experimental group that receives the new treatment and a control group that does not.

To avoid possible bias in interpreting the results, randomized trials are generally double blind; that is, neither doctors nor patients know who is receiving the treatment and who is not. Patients in the control group may be given a placebo (inactive substance) that resembles the new drug in appearance so that no individual will know whether they are in the control group or the experimental group.

The purpose is to control for the placebo effect, which is any beneficial effect on a patient’s condition that may be caused by a person’s expectations concerning a drug rather than by the drug itself. Placebos, however, are not used to substitute for currently existing treatments that are known to be beneficial.

For example, the experimental group might receive the standard treatment along with the new drug, while the control group receives the standard treatment along with a placebo.

Based on the results of Phase III randomized trials, the FDA decides whether or not to approve a new drug as an acceptable treatment for standard medical use. After approval has been granted, further Phase IV clinical trials may be carried out to answer additional questions concerning the best ways to use the drug or to explore possible side effects that were not detected in earlier testing.

26. Essay on Cancer Treatment: (Around 640 Words)

Complementary and Alternative Cancer Treatments are Frequently Used by People who have Cancer :

Prior to obtaining FDA approval, new drugs undergoing laboratory and clinical testing are referred to as experimental treatments. It usually takes many years to obtain enough evidence to justify incorporating an experimental treatment into standard medical practice. In addition to experimental treatments, a diverse array of unproven and largely untested cancer treatments exists that are not part of standard medical practice.

These treatments can be subdivided into complementary treatments, which are used along with standard medical care, and alternative treatments, which are used as a substitute for standard medical care.

Complementary and alternative treatments include herbal remedies, vitamins, special diets, and a variety of physical and psychological practices such as massage and relaxation techniques. More than half of all individuals with cancer have been reported to use one of more of these practices, often without discussing it with their doctor.

Complementary treatments are usually used to control symptoms and improve a person’s quality of life while under standard medical care. In contrast, many alternative treatments are claimed to cure cancer. Individuals who rely solely on these alternative remedies may put themselves at considerable risk.

A striking example is provided by the history of laetrile (also called amygdalin or vitamin B17), a natural substance extracted from apricot pits that attracted considerable attention in the 1970s when medical clinics in Mexico claimed that it cured cancer. Research in laboratory animals failed to show any anticancer effects of laetrile, so it did not meet the normal standards for human testing in the United States.

However, the prominence of laetrile and its use by thousands of Americans (many of whom traveled to Mexico for treatment) led the National Cancer Institute to sponsor a human clinical trial despite the absence of supporting data from animal testing. After the trial showed laetrile to be ineffective against cancer, its popularity gradually declined.

In retrospect, the lack of anticancer properties was not the only problem with laetrile. The drug also has hidden dangers because it breaks down to form cyanide, and some people treated with laetrile may have died of cyanide poisoning rather than their cancers.

Another risk incurred by individuals who rely on unproven remedies such as laetrile is that they deny themselves the benefits of any proven methods that may be genuinely useful for their particular type of cancer.

Although the experience with laetrile highlights the need for caution, it does not mean that alternative remedies are always risky and without value. An intriguing example involves an herbal product called PC-SPES (“PC” for Prostate Cancer and “SPES” from the Latin word for “hope”).

PC-SPES, which consists of extracts from eight herbs, was introduced in 1996 as a remedy for prostate cancer. Because it was being sold as a dietary supplement consisting entirely of natural ingredients, PC-SPES did not require a doctor’s prescription or fall under governmental regulations for purity or effectiveness.

Shortly after it was introduced, several studies reported that PC-SPES slowed the growth of prostate cancer in humans (Figure 20). These encouraging results made PC-SPES one of the best prospects for an alternative cancer treatment that might stand up to the scrutiny of rigorous scientific testing.

However, chemical analyses of PC-SPES subsequently revealed that this supposedly “all natural” herbal mixture was contaminated with several synthetic drugs, and the manufacturer voluntarily stopped selling it.

When it was discovered that several other herbal products sold by the same company were also adulterated with synthetic drugs, the company went out of business and PC-SPES is no longer available today.

This cautionary tale illustrates the problems that arise when trying to evaluate the possible effectiveness of herbal remedies, which are not subject to the kinds of strict governmental regulations for purity, composition, and effectiveness that apply to the drugs manufactured by pharmaceutical companies.

27. Essay on Cancer Treatment: (Around 400 Words)

Psychological Factors are not a Significant Cause of Cancer but may Influence the Course of the Disease :

Cancer patients who have been treated with placebos in clinical trials sometimes exhibit improvement in symptoms such as pain and poor appetite. Since placebos contain no active ingredients, this phenomenon raises the question of the relationship between psychological factors and cancer.

Numerous investigations into the role of psychological factors have been carried out over the years, with special attention paid to stress and depression because both can trigger changes in the immune system.

Early studies revealed that cancer patients are more likely than other individuals to be depressed and anxious, which was initially interpreted to mean that psychological stress can cause cancer. A more straightforward interpretation, however, is that depression and anxiety are triggered by the discovery that a person has cancer, occurring after the disease arises rather than being the underlying cause.

Large prospective studies in which psychological traits are measured in healthy individuals who are then followed into the future to see who develops cancer have generally failed to support the idea that psychological factors are a significant cause of cancer. Some studies have documented an increased rate of cancer deaths among people who have recently experienced a highly stressful or depressing event, such as the loss of a spouse or other close family member.

However, cancer typically takes ten or more years to develop, so these cancer deaths are likely to involve tumors that were already growing in the body at the time of the psychological disturbance (even if the disease had not yet been diagnosed). The overall body of evidence therefore suggests that psychological factors are not a significant cause of cancer, but they may influence the course of the disease after it has already begun.

If that is true, it raises the question of whether psychological interventions might be beneficial for cancer patients. In 1989, a widely publicized study reported that women with advanced breast cancer who participated in cancer support groups lived about 18 months longer than women who did not.

Although these findings were widely accepted at the time, subsequent studies have failed to confirm the conclusion that cancer patients participating in support groups live longer than nonparticipating patients.

Support group participation is, however, consistently associated with improvements in patients’ awareness about their illness and reductions in anxiety and distress. Whether support groups or other types of psychological intervention can extend survival for certain individuals remains an open question.

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The students and postdoctoral researchers who work and train in MSK’s laboratories drive discovery forward every day. Today they are vital partners. Tomorrow they will lead further progress at hospitals, research centers, and biomedical companies around the world.

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Second Cancers

One to three percent of survivors develop a second cancer different from the originally treated cancer. The level of risk is small, and greater numbers of survivors are living longer due to improvements in treatment. However, even thinking about the possibility of having a second cancer can be stressful.

Current research shows that cancer survivors in general have an increased chance of developing cancer compared to people of the same age and gender who have not had cancer. This means that it is even more important for cancer survivors to be aware of the risk factors for second cancers and maintain good follow-up health care.

Develop a Survivorship Care Plan

Know your treatment history. This includes an understanding about your specific type of cancer and the amount of chemotherapy you received. It is also important to know about the location and the amount of (dose) of the radiation treatment you received.
Work with your health care provider to develop a survivorship care plan with recommendations for follow-up care.
Develop a schedule for screening exams and regular screening and check-ups with your health care team.

Risk Factors for Second Cancers

Whether or not you will have a second cancer depends on many different things. This may include your age when treated, the treatment you received and your genetic make-up and family history. Even if you find you are at a higher risk, it does not mean that you will develop cancer again. Keep in mind that, although the risk is higher, the actual number of people who will get a second cancer is relatively small. Each cancer survivor’s experience is unique. This overview describes some of the risks for developing second cancers:

Type of cancer: The type of original cancer you had may affect your risk for a second cancer because some cancers require treatment with radiation or high doses of certain types of chemotherapy. It is not yet clear to researchers if the second cancer is caused by the treatment or by the original cancer, or by a combination of the two. Another possibility is that both the original cancer and a second cancer share certain risk factors such as an underlying cause, environmental exposure or genetic predisposition.
Age at time of treatment: Children and young adults have a higher risk of second cancers related to treatment with radiation or chemotherapy than older adults have. Younger survivors have more at-risk years for second cancers. Generally, you should always be alert for symptoms of a second cancer.With age, the risk of cancer increases even among those who have never had cancer. Researchers continue to study second cancers in survivors. They hope to develop treatment methods that reduce the risk of developing cancer again. A healthy lifestyle may help minimize this risk.
Procarbazine.
Mechlorethamine.
Chlorambucil.
BCNU (bischloroethylnitrosourea).
Nitrogen mustard.
Cyclophosphamide.
Ifosfamide.
Epipodophyllotoxins.
Anthracyclines.
Type of radiation: The higher the dose of radiation received, the more risk for developing a second cancer. In general, the risk of having a second cancer from radiation is very low, and much depends on the amount of radiation given during treatment. For survivors of childhood cancer, radiation therapy is the most important risk factor for second cancers.
Bone marrow transplant: With longer follow-up of increasing numbers of survivors after hematopoietic stem cell transplant (SCT), there may be an increased risk of second cancer. This may be related chemotherapy and radiation treatments, effects on the immune system and genetic predisposition.
Family history: When cancer “runs in the family,” survivors have a higher chance of developing second cancers than those who do not have a family history of cancer. Survivors from families who have “predisposing conditions” that increase the possibility of cancer should know their family history. They should also participate in specialized follow-up care that can help with early detection.
Lifestyle: Smoking, excessive alcohol use, lack of exercise and poor diet are some of the unhealthy behaviors that might be risk factors for second cancers. These are the only known risk factors for a second cancer that you can personally avoid by choosing to change some of the habits that put you at risk.

Sometimes second cancers happen in survivors who were not affected by any of the risk factors mentioned above. Ask your health care provider to discuss your risk factors for a second cancer based on your cancer type, treatment received and your general medical history.

Keep Track of Your Family History

If there is a history of cancer in your family, it is especially important to understand risk factors and have regular screenings. Your health care team can help you decide if genetic counseling or testing is recommended.
If you do not know about your genetic background, start talking with relatives or friends who know your family’s medical history. In many cases, no one has written down the information and only an oral history is known. You can begin to develop these records for yourself. It may also be helpful to other members of your family.

Maintain a Healthy Lifestyle

Avoiding tobacco products.
Working with your health care team to develop an exercise plan.
Maintaining a healthy body weight.
Eating five to seven servings of fruits and vegetables a day.
Performing regular breast or testicular self-exams and skin exams each month.
Using sunscreen and avoiding exposure to the sun, particularly on irradiated skin.
Getting enough rest and sleep.

Symptoms of Second Cancers

Knowing the general symptoms of cancer is a great way to help you detect a second cancer early. The earlier a second cancer is diagnosed, the more likely it can be successfully treated. In some cases, second cancers cannot be prevented.

Some types of cancer may not present any symptoms. Health care including regular check-ups and screenings can help detect problems early. Screening may include blood tests and imaging such as X-rays, CT scans and PET scans.

Symptoms include:

Changes in bowel or bladder habits.
A sore that does not heal.
Unusual bleeding or discharge.
Thickening or lump in the breast or other parts of your body.
Indigestion or difficulty swallowing.
Noticeable change in a wart or mole.
Nagging cough or hoarseness.
Changes in vision.
Constant or severe headaches.

Having some of these symptoms doesn’t mean you have cancer. However, it’s best to talk with your health care provider if you notice these or other symptoms. Open communication with your health care team may help them recognize signs or symptoms that are not always easy to see on your own. Also, talking with your doctor about concerns you have about second cancers may help relieve some of the anxiety that you might have.

Does Cancer Treatment Cause Second Cancers?

No one knows exactly why survivors who have been treated for cancer develop a second cancer. Yet, there are some theories about why cancer and its treatment sometimes cause second cancers including:

Some research suggests that chemotherapy and radiation may weaken the immune system making it easier for second cancers to develop.
Sometimes chemotherapy that is used to treat the original cancer may cause the bone marrow to make abnormal cells. This might lead to second cancers in some survivors.
Radiation destroys cancer cells and may cause damage to healthy cells. This damage may contribute to second cancers.

Your health care team has a primary goal of treating the cancer the best way they can. Research is ongoing to create treatment options for survivors that decrease the risk of long-term effects and improve the quality of life for survivors.

In the past, some second cancers were caused by treatments that are no longer given today. Newer treatments for cancer generally use less toxic medicine than was used years ago. Research may show that this will ultimately result in a decrease in the number of second cancers that develop in survivors.

When Do Second Cancers Occur?

A second cancer can appear at any time during survivorship. Some studies show that a common time for cancers to develop is from five to nine years after completion of treatment.

For childhood cancer survivors, secondary leukemia is most likely to occur less than ten years after treatment of the original cancer. Solid tumors related to radiation may occur more than ten years afterward. However, because the exact causes of second cancers are not yet known, it is difficult to predict when they might appear. Lifetime monitoring by health care providers who are knowledgeable about survivorship care is recommended—even years after completing treatment for the original cancer.

Minimize the Risk of Second Cancers

One of the most important things you can do is to follow-up with a health care team that is well-informed about survivorship care. Good medical care and screening can help detect second cancers early.

Try to find balance with a healthy lifestyle.
Know if your family has a history of cancer.
Use a health journal to prepare for your next visit with a member of your health care team.

Keep Track of Your Health Care

Keep a health journal.
Write down everything you want to ask your health care team. Take notes and keep track of questions between visits.
Make a list of your medications. Bring this information to the visit along with all of your medication bottles. This will help the health care team keep track of all the medications you are taking, including vitamins and over-the-counter medications.
Take notes during health care appointments.
Keep all of your health records together and bring this information with you to health care appointments.
Bring extra copies of important documents to give to appropriate health care team members. You can also fax or mail these before your appointment. Having the health care team read your documents may be an easier way for you to communicate.
Store pamphlets, information about medication side effects and important phone numbers in your notebook so that everything is in one place.

Fear of Cancer Recurrence

Fear of recurrence, the concern that cancer will come back after treatment, is common among survivors. Although having some concerns about recurrence is natural, too much worrying can affect your quality of life. Understanding how to manage fear of recurrence can help you feel more confident and secure about survivorship. If you experience this type of fear:

Talk with your friends and loved ones about your concerns. You might find that beginning a conversation about your fears can be helpful for loved ones and friends. Some may be afraid to bring up their worries because they don’t want to upset you. However, talking with them may help them, and you are likely to feel less alone. Together, you may be able to come up with a plan to face these fears.
Find a cancer support group. Support groups can provide a safe environment to share experiences with other survivors. You can also learn new ways to handle difficult situations and have a chance to talk about emotional issues that only survivors may understand. These groups can offer an opportunity to learn different styles of coping with fear and ways of adjusting to life as a cancer survivor. If you are not comfortable talking about certain subjects with your family or friends, a support group will offer a place to talk freely about what is important to you. Each support group is unique so you may want to try more than one to find the best one for you.
Talk with a professional therapist. If family and friends are not able to help you with concerns, your health care team or a licensed counselor may be an important source of support. Ask for a referral to a therapist who works with other cancer survivors. Most cancer centers employ oncology social workers who are specially trained to work with cancer survivors and their families. Even if you are not a patient at a cancer center, the oncology social worker may meet with you or refer you to someone else in the community.

No matter how long it has been since you finished treatment, there may be certain occasions when the fear of cancer recurrence affects you. With time, you are likely to find that your concerns and the level of fear may lessen.

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Survivor Interview – Terry H.

Terry is a leukemia survivor. He discusses dealing with the aftereffects of chemotherapy, dating, and his relationship with his family.

Survivor Interview – Elizabeth M.

Elizabeth was diagnosed with chondrosarcoma of the pelvis. She discusses emotional support, aftereffects of treatment, and chronic pain.

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JSmol Viewer

A patient-centered conceptual model of aya cancer survivorship care informed by a qualitative interview study.

Simple Summary

1. introduction, 2.1. recruitment, 2.2. interview approach, 2.3. analysis, 3.1. overall themes, 3.2. care coordination and healthcare system navigation support.

“So there really wasn’t much time. Or was there? I didn’t know to ask that question. Okay, I know this is growing—is there enough time for me to get a consultation? I don’t know if maybe I could have waited a few days. I just don’t know, because I didn’t know that question to ask... But I just went ahead and signed away because I felt like I was—I hate to say the word bullied, but I felt like I was in a corner. I was like oh my god—this cancer’s bigger than me, just get it out, kill it! Do what you need to do.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“I, I mostly blamed myself for my inexperience in hospitals, I guess. But yeah, I felt like people weren’t necessarily completely clear, well, telling me exactly what I had to do. What I should do. Like when I should ask for help or when I didn’t need to, that sort of thing.”— Participant 2, female, renal cell carcinoma, 30–39 years old at diagnosis .

“I felt like I had to be the care coordinator. I had to make sure everybody knew what the other was doing. Proactively ask for appointments—like okay, I’m going to have to get radiation next. And they’re like oh, you can wait for that until the week before, and I was like, but what if I don’t like [the provider]? You’re going to put me in a box. So I had to just be proactive to get the kind of care that I wanted to get. And I felt like my care coordinator, which is exhausting.”— Participant 4, female, breast cancer, 30–39 years old at diagnosis .

“I was first getting treatment somewhere and I didn’t feel completely taken care of there. As a nurse practitioner, I felt like I was asking—I was supposed to be a patient then, I wasn’t supposed to be a health care provider. So I felt like I was directing my care and I was reminding them of things. It didn’t feel like the right fit for me with my oncologist and the care team, so I ended up after getting a second opinion switching to another hospital.”— Participant 3, female, Hodgkin’s lymphoma, 20–29 years old at diagnosis .

“Gosh, that’s really why I became an advocate—I just couldn’t believe the lack of treating me as a holistic person. I understand that I guess to be an oncologist you’re going to meet patients who ultimately die from it, and I get that they’re trying to make sure that you don’t die, and that is of course great, you kind of need that. But what about a nurse navigator or even like the nurse? There was no follow up... there needs to be a middle person. Whether it be that nurse or that social worker, and it should be mandatory that every AYA... have an initial conversation [with them] and then determine if you want to work with them...The follow ups just go through the cracks.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“I felt like my oncologist was very good at giving me medications to deal with nausea and other side effects when I needed them...But I had to research online what are things that I could use and then go and ask for it, as opposed to someone presenting me with “these are all the resources” or “these are things you should consider, let us know what you need”. I felt like the latter would have been much more helpful. I went to [other specialty cancer centers, and] both of those hospitals did provide that. Like “here’s your coordinator, here’s a whole pamphlet, here’s all the resources we have. Here’s how you use each one”. So I thought that was really cool.”— Participant 4, female, breast cancer, 30–39 years old at diagnosis .

3.3. Mental Health Support

“Definitely anxiety, depression for sure. I think those would be the biggest two that I’ve had to deal with. It’s an everyday struggle … Anxious about my cancer getting worse or also having cancer in my family or friends, since I already know what it feels like, having cancer. I wouldn’t want any of my loved ones to go through the same thing.”— Participant 6, female, breast cancer, 30–39 years old at diagnosis .

“Cancer is trauma, and even though a lot may not equate it with that term, because they just don’t know, a lot of us have PTSD. And that’s not talked about enough… every experience in the AYA community matters. So that might be why someone would not [talk to a researcher about their cancer experience], because they might feel like you could talk to someone better. It’s really about insecurity, but also too how they’ve been treated throughout their treatment. It can be hard to discuss and be traumatic. I can now verbally talk about it without bursting into tears, but not everyone can.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“Obviously having cancer kind of like fucks you up mentally. But I’ve been going to therapy, I actually take an antianxiety med now.”— Participant 8, female, Hodgkin’s lymphoma, 15–19 years old at diagnosis .

“Like I thought, I thought I was alone for like five years … Post treatment I actually had a really bad depressive episode, because I was just in such despair because I thought I was alone and no one else was like me. And I did hours of searching and finally found a couple of organizations that led me to other things. But I would have liked to have those resources [earlier], I wouldn’t have felt so alone.”— Participant 8, female, Hodgkin’s lymphoma, 15–19 years old at diagnosis .

“I actually learned about the support groups from Instagram … just as a young Black woman, [it was important] to see other women of color that were young and that looked like me, because I was not seeing that at my cancer center. So that was a huge support for me. Also, just by sharing my story, it allowed me to pay it forward to other young adults and also inspired me to get involved in advocacy work.”— Participant 9, female, breast cancer, 30–39 years old at diagnosis .

3.4. Peer Support and Making “Cancer Friends”

“It’s bad enough I’m an AYA, it’s bad enough I’m Black, it’s bad enough I’m a woman, it’s bad enough that I am an only child. I feel like all of these things were hitting me—and I have cancer, and now I literally have no one? It’s been hard.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“So, I think at the time the quintessential experience of being the youngest person at the cancer center in the waiting room, you know, not seeing anybody else my age unless they were in a caregiver capacity... And just feeling like I was the only person my age that had cancer and was getting treatment. And so the experience was very different when you are under 40. I didn’t know other people that had gone through that at the time.”— Participant 10, male, testicular cancer, 30–39 years old at diagnosis .

“As I was nearing the end of chemotherapy, I was feeling like I couldn’t really talk to my friends the same, and I didn’t really have people to relate to, and I felt like an astronaut. My brain was foggy, I really wanted to talk to someone about [my side effects and stuff] without worrying people. I remember Stupid Cancer was the big [AYA organization] at the time, and I saw that they had in-person Meetups. I decided to go … and then I instantly was like oh, maybe this [is] a window into a community I didn’t even know existed. I didn’t picture people in their 20s and 30s with cancer hanging out before this. That was the beginning of making cancer friends, [we have fun but] also if someone does need to vent about their situation, treatment, insurance, or relationships going away because of cancer, you’re the perfect [person] to talk to about it.”— Participant 11, male, testicular cancer, 30–39 years old at diagnosis .

“I went through a lot of side effects. I literally had the motherlode of side effects and what was very hurtful was when my oncologist would be like yeah, you know, a lot of patients get that. Well, it’s my first time seeing my tongue turn black, so you might want to have some sort of—I don’t know, like compassion for how freaked out I would be. Even my throat would swell and I had difficulty swallowing. ‘Oh, I’ve seen it before, I’ve seen worse.’ Well, I’ve never seen worse.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“I wish that that there was an AYA program at the hospital to tell me about these resources. To tell me like, hey, there’s a Gilda’s Club, it’s 10 to 15 min from here. There’s a meeting once a month. You can go and meet people your own age. It’s safe. People are really cool. Check it out. And now you can join these virtually. Just having somebody to say to me that is totally normal to feel that way. There are other people your age that get treatment here and you can meet them. That would have been really awesome.”— Participant 10, male, testicular cancer, 30–39 years old at diagnosis .

“I think just introducing for patients, that adolescent young adult oncology exists, and there is support out there for AYA’s. I didn’t really dive into the AYA support community until after treatment and got connected to a lot of resources and a lot of friends that way. But I think if I had known that resources like that existed while I was going through treatment, it would have been helpful just to know that I wasn’t alone and all these amazing organizations exist.”— Participant 12, female, osteosarcoma, 15–19 years old at diagnosis .

3.5. Empathic Communication about Fertility Preservation

“When I got diagnosed in the hospital … they had brought in a blood specialist and he described leukemia to me … After he left one of the interns immediately asked me, like so do you have any kids? And I was like no. And he was like, have you thought about freezing your eggs? And I’m like, dude, this dude just told me about cancer, like I haven’t, I can’t talk about kids right now like. You know?”— Participant 13, female, leukemia, 20–29 years old at diagnosis .

“The timing was rushed because it was overwhelming. I feel like if you sit down with anybody, man, woman, whatever, and tell them you might not be able to have kids, that’s pretty heavy and something you want to sit with. And … it’s not like it was free to go get the sperm banking done and have it stored. But I was like well, if I don’t do this, that might be it, I might never have kids. Even if I don’t want them at the moment, taking the option off just seemed scary. So yeah, I would have liked to have had more time.”— Participant 11, male, testicular cancer, 30–39 years old at diagnosis .

“Everything for me happened within like three days, so there was no, no ability to like, I don’t even know what it’s called. But to … freeze my eggs, I didn’t have that option because of the type of cancer I had everything had to be done so quickly. The only thing I was told in regards to fertility is you may not be able to have kids. There’s a high likelihood with the chemotherapy you are receiving that you may not be able to have children after this. There was no offering of like any type of resources. I only found that out afterwards, [about] all like the different type of programs for patients.”— Participant 15, female, leukemia, 20–29 years old at diagnosis .

“We talked about [fertility preservation] in [my support] group before and I guess, well, I mean for guys it’s easy, so they’re super on top of it as far as when we spoke about it. But a lot of [women] who were in similar positions to me where it was all just really sad. From my experience [the doctors] were like, okay, you’re here now, here’s your doctor, here’s your treatment. Oh, by the way there’s this [fertility preservation option], we kind of want to get started right now, so could you just not [have kids] … It wasn’t a huge deal, but I was a little sad.”— Participant 14, female, leukemia, 20–29 years old at diagnosis .

“There should have been a follow up call [after my diagnosis]. Because that was a really intense moment. My first time as the patient … Why wasn’t there a follow up? Like hey, I know you just heard a lot of information, let’s talk about this. I feel like I should have at least been required to get a consultation with an infertility specialist, even though it wouldn’t have been covered under my insurance. I feel that conversation should at least have been had so they could make sure I was really making the best decision for myself at that time. Sorry, I get really passionate and very angered about it.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“I lost my fertility. No one prepared me for that. I didn’t receive initial counseling going into that surgery or coming out of it. I didn’t expect to experience that kind of grief, because I was single all this time, and childless, and now I am chronically single and barren forever. None of my doctors cared to see how that would affect me.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

“I don’t really have trouble communicating with [doctors]. I’m a lawyer and I did a lot of research, so I generally got the comments that ‘oh, you’re so knowledgeable, you’re an easy patient.’ [But] I don’t think they necessarily answered all my questions, or gave me all the resources that were available, or were upfront about side effects, which I found frustrating…[the doctors failed] to mention fertility resources [so] I found my own stuff … I certainly wouldn’t say I got most of my information from my oncologist, but I found it in other places.”— Participant 4, female, breast cancer, 30–39 years old at diagnosis .

“My oncologist is very respectful of my wishes in terms of wanting to have another baby … but then [she] also wasn’t afraid to tell me, you know, we can only do one round of harvesting your eggs, because it’s not safe to do more. She did a really good job acknowledging my dream and weighing that accordingly, [so] I’m not risking life … but I’m still able to try to, you know, preserve my fertility before having this definitive surgery.”— Participant 5, female, ovarian cancer, 30–39 years old at diagnosis .

“Before I started chemo, my social worker came to talk to me in the hospital room and she just wanted me to know like hey, your doctors want you to do chemo, but you don’t have to do it right now, you can work on the fertility thing, if it’s important to you. So she made me feel comfortable that it was okay to delay the treatment.”— Participant 7, female, leukemia, 20–29 years old at diagnosis .

3.6. Financial Burden and Need for Support

“We needed help, we had help from family and friends, but again, the financial burden … is just a nightmare. You got the financial burden, you got the paperwork. You’re supposed to be focusing on your health.”— Participant 5, female, ovarian cancer, 30–39 years old at diagnosis .

“I worked in fine dining and didn’t have any insurance … And then the diagnosis alone racked up I think tens of thousands of [dollars in] debt and I was just through biopsies and scans and you know. I was going to, which is laughable, but it was called free clinic. It took a long time before I was diagnosed; go get bloodwork, come back in two weeks, schedule another appointment for two weeks later. And debt was mounting.”— Participant 16, male, Hodgkin’s lymphoma, 20–29 years old at diagnosis .

“I probably know more about the American health services than I ever wanted to know … it’s just not the way I would have liked to have learned it.”— Participant 8, female, Hodgkin’s lymphoma, 15–19 years old at diagnosis .

“With my age I am able to be on my dad’s insurance and it is a really good insurance plan. So it hasn’t been like insanely expensive or anything … But as I approach my 26th birthday, the cutoff [of staying on my parents’ insurance], I have lots of concerns with finding good health care on my own.”— Participant 14, female, leukemia, 20–29 years old at diagnosis .

3.7. Quality of Life

“When I was first diagnosed I was studying for a board license for civil engineering. I was still thinking I’m going to be in chemo for eight hours, I’ll have a lot of time to study at the hospital. It wasn’t like that at all. That’s when I was in denial, and I think after that, that’s when depression hit me. I was like you know what? It’s over, I’m just going to keep my job now. There’s no way I can study for the exam … Sometimes in my back of my mind I’m still thinking I want to be a licensed engineer and all I have to do is pass that exam. I start dreaming that when I pass the exam, I’m going to get my promotion and travel more, which I used to do before diagnosis … I guess career-wise I still think about getting my license, even if I don’t keep working in the engineering field, I want to feel accomplished. I want to be able to say even through or despite cancer, I was still able to accomplish that.”— Participant 6, female, breast cancer, 30–39 years old at diagnosis .

“So because I got sick, at least with my internship hours, I could have been done last December. But I was going through treatment. And my friend and I were collecting hours and going to school at the same time. She already finished herself, got certified, she’s my boss right now. She’s my supervisor. We were like at the same level, she’s already above me. So and she doesn’t treat me any lower, but I’m still a little upset sometimes because I could have been there by now if I hadn’t gotten sick.”— Participant 13, female, leukemia, 20–29 years old at diagnosis .

“I’ve been a dog groomer on and off for about 10 years. And I when I was finally able to get back into work [right after my surgery], I felt like they didn’t understand what I was going through. Like I was very anxious, and there’s a lot of sounds in a grooming salon. And it was really putting me on edge. And I started to wear earplugs to deal with that. And then I started getting like looks from my coworkers and like I just started to feel less and less welcome there. And I just gave up on it and I ended up quitting that job. I just didn’t feel very good there anymore.”— Participant 2, female, renal cell carcinoma, 30–39 years old at diagnosis .

“I did officially go back up to my regular hours, but there are some days that I take time off for appointments. I try to schedule for example my scans in one day, for example, so I only have to take one day off whenever I can…It’s not just cancer that we deal with, we still have to deal with what other people go through as well, for example taking time out for dental and eye doctor appointments. I still have to take time off for that.”— Participant 6, female, breast cancer, 30–39 years old at diagnosis .

“I had never been to the hospital before. And so I had to go through getting my diagnosis. Going through all these different procedures. And every one alone. They transferred me because they didn’t have the resources where I live to treat me. They transferred me to Houston, so my life got uprooted. My job put on hold. I had to move about five hours away so I could get treatment.”— Participant 13, female, leukemia, 20–29 years old at diagnosis .

3.8. Information about and Support Mitigating Side Effects and Late Effects

“The important elements for young adult cancer care compared to the typical cancer patient that you think of, like 50, 60, 70, they’re worried more about the here and now, and they don’t necessarily have to worry about side effects 20, 30 years down the road, because life expectancy, they won’t be there. I was diagnosed at 25. God willing, I’ll be alive for 50 more years beyond that. I don’t want to be dealing with side effects for years on end, so if there’s an option that’s a little bit more conservative treatment, which will possibly result in less side effects but maybe instead of saying it’s 100% certain, it’s 80% certain. That’s a 20% difference, so I think addressing that in terms that are easily understood by young adults, and also not in a talk down to manner, is super important.”— Participant 17, male, testicular cancer, 20–29 years old at diagnosis .

“Oh, and then the thing I always forget are the other secondary effects of treatment. I had to have both shoulders and both hips replaced, and I had no idea that was going to be in my future whatsoever, at the time of treatment.”— Participant 18, female, leukemia, 20–29 years old at diagnosis .

“I have osteoporosis and I’m not even 25 yet, so that’s kind of concerning for the future.”— Participant 14, female, leukemia, 20–29 years old at diagnosis .

“The one thing I do deal with is, because of all the surgery I’ve had, I have chronic nerve pain, nerve damage, so that’s not fun to deal with. I wish I would have known that it was a possibility, because I was not told that it was a possibility that this could happen.”— Participant 19, female, sarcoma, 15–19 years old at diagnosis .

“I’ve got major issues with the majority of my organs. I have liver damage. I have heart failure. I was in a wheelchair for a while. I was on bedrest for a very long time right after everything. I am disabled. I am on disability. And I do not have the energy I once did. Napping and every couple days just being totally exhausted is kind of part of my life.”— Participant 20, female, leukemia, 30–39 years old at diagnosis .

“I have permanent damage—I don’t feel my feet, my toes from the upper balls to my toes. Sometimes the numbness goes up my legs… and I’ve fallen, actually almost fractured my ankle in January because I didn’t feel my foot. It was so sudden and severe, and … no one seemed to take it as seriously as I did, which is frustrating.”— Participant 1, female, breast cancer, 30–39 years old at diagnosis .

3.9. Attention to the Unique Needs of Young Adults

“[My center had] an AYA program. Granted, they have so much volume because they have a special unit, so I think volume begets resources. But they have providers who are knowledgeable and not just oncologists, but lots of different providers who are knowledgeable about issues that AYA’s face, especially fertility. Sometimes we respond differently to drugs. If every center could have somebody who has a special research focus, to keep up to date on AYA’s. Or a pamphlet, a website, that even would have been helpful. I feel like there’s many ways to skin the cat, but it’s just providing age-appropriate information.”— Participant 4, female, breast cancer, 30–39 years old at diagnosis .

“But I definitely wanted more [young adult] support specifically. And not just in general cancer support, I went through this huge ordeal; it’s completely life changing. And I just, to me the more support I’m getting I feel more in control and I have more power.”— Participant 5, female, ovarian cancer, 30–39 years old at diagnosis .

4. Discussion

4.1. care coordination and healthcare system navigation, 4.2. mental health support, 4.3. aya peer support, 4.4. empathic communication about fertility preservation, 4.5. financial burden, 4.6. quality of life, 4.7. education and support regarding side effects and late effects, 4.8. attention to the unique needs of young adults, 4.9. limitations, 4.10. implications for cancer survivors, 5. conclusions, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, acknowledgments, conflicts of interest.

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Click here to enlarge figure

	Number (%)

Female	21 (84)
Male	4 (16)

White	19 (76)
Black	2 (8)
Middle Eastern/North African	1 (4)
Other	3 (12)

Hispanic/Latinx	6 (24)
Not Hispanic/Latine/x	19 (76)

20–29	8 (32)
30–39	12 (48)
40–49	5 (20)

15–19	4 (16)
20–29	10 (40)
30–39	11 (44)

Less than 2 years	3 (12)
At least 2, but less than 5 years	8 (32)
At least 5, but less than 10 years	11 (44)
10 or more years	3 (12)

Less than 2 years	5 (20)
More than 2, but less than 5 years	12 (48)
More than 5, but less than 10 years	5 (20)
10 or more years	3 (12)

Breast	5 (20)
Chromophobe Renal Cell Carcinoma	1 (4)
Hodgkin’s Lymphoma	4 (16)
Leukemia	7 (28)
Lung	1 (4)
Myelodysplastic Syndromes (MDS)	1 (4)
Osteosarcoma	1 (4)
Ovarian	1 (4)
Sarcoma	1 (4)
Testicular	3 (12)

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Figueroa Gray, M.S.; Shapiro, L.; Dorsey, C.N.; Randall, S.; Casperson, M.; Chawla, N.; Zebrack, B.; Fujii, M.M.; Hahn, E.E.; Keegan, T.H.M.; et al. A Patient-Centered Conceptual Model of AYA Cancer Survivorship Care Informed by a Qualitative Interview Study. Cancers 2024 , 16 , 3073. https://doi.org/10.3390/cancers16173073

Figueroa Gray MS, Shapiro L, Dorsey CN, Randall S, Casperson M, Chawla N, Zebrack B, Fujii MM, Hahn EE, Keegan THM, et al. A Patient-Centered Conceptual Model of AYA Cancer Survivorship Care Informed by a Qualitative Interview Study. Cancers . 2024; 16(17):3073. https://doi.org/10.3390/cancers16173073

Figueroa Gray, Marlaine S., Lily Shapiro, Caitlin N. Dorsey, Sarah Randall, Mallory Casperson, Neetu Chawla, Brad Zebrack, Monica M. Fujii, Erin E. Hahn, Theresa H. M. Keegan, and et al. 2024. "A Patient-Centered Conceptual Model of AYA Cancer Survivorship Care Informed by a Qualitative Interview Study" Cancers 16, no. 17: 3073. https://doi.org/10.3390/cancers16173073

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Scientists discover how the body's killer cells attack cancer

Scientists are on the verge of a cancer breakthrough after working out how the body's immune system targets cells devastated by the disease.

A new study has discovered that our natural killer cells, from the immune system which protect against disease and infections, instinctively recognise and attack a protein that drives cancer growth.

The experts say that by hijacking this protein, known as XPO1, they may be able to activate more killer cells to destroy the disease.

Scientists from the University of Southampton, working with experts worldwide, led the study and now believe it could offer new and less invasive forms of treatments.

The findings have been published in the Science Advances journal.

Lead author Professor of Hepatology Salim Khakoo, from Southampton, said it was previously believed that killer cells attack cancer cells in a random manner.

He added: "Our findings actually show how our body's immune system recognises and attacks these cancer cells.

"Killer cells are an emerging form of immunotherapy that shows huge promise.

"They don't attack healthy tissue in the way chemotherapy and other immunotherapies do, so are safer and have less side-effects than traditional forms of cancer treatment."

The XPO1 protein examined by the scientists is essential for normal cell function.

However, in many cancers, it becomes overactive and allows malignant cells to multiply unchecked.

The Southampton scientists found that a peptide -- short chains of amino acids -- derived from the XPO1 protein attracted the natural killer cells.

This, they say, triggers the body's immune response against the cancerous cells.

Prof Khakoo added: "Patients with cancer who had both active killer cells and high levels of XPO1 had significantly better survival rates.

"This holds true for a range of cancers including those with higher rates of death such as liver cancer, which has an average survival rate of only 18 months.

"As well as liver cancer, killer cell treatment in the future could be used to treat head and neck cancers, endometrial, bladder or breast cancer."

Previous studies have linked natural killer cells to the body's protection against cancer.

But the latest study is the first of its kind to highlight a viable technique of activating killer cells -- to target the XPO1 protein -- to fight the disease.

Co-author Professor Ralf Schittenhelm, from Monash University in Australia, said the discovery could change the course of immunotherapy.

"We hope it could lead to personalised cancer treatment, especially in cases where traditional therapies have failed.

"The potential to develop targeted therapies that utilise the body's own immune system is incredibly exciting."

The scientific team at Southampton are now working on the development of the world's first vaccine that uses natural killer cells to fight cancer.

Immune System
Brain Tumor
Skin Cancer
Colon Cancer
Prostate Cancer
Lung Cancer
Immune system
Natural killer cell
Chemotherapy
Monoclonal antibody therapy
Prostate cancer
White blood cell

Story Source:

Materials provided by University of Southampton . Note: Content may be edited for style and length.

Journal Reference :

Matthew D. Blunt, Hayden Fisher, Ralf B. Schittenhelm, Berenice Mbiribindi, Rebecca Fulton, Sajida Khan, Laura Espana-Serrano, Lara V. Graham, Leidy Bastidas-Legarda, Daniel Burns, Sophie M.S. Khakoo, Salah Mansour, Jonathan W. Essex, Rochelle Ayala, Jayajit Das, Anthony W. Purcell, Salim I. Khakoo. The nuclear export protein XPO1 provides a peptide ligand for natural killer cells . Science Advances , 2024; 10 (34) DOI: 10.1126/sciadv.ado6566

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An in silico investigation on the binding site preference of PD-1 and PD-L1 for designing antibodies for targeted cancer therapy

Abdolmaleki, Sarah
Ganjalikhani hakemi, Mazdak
Ganjalikhany, Mohamad Reza

Cancer control and treatment remain a significant challenge in cancer therapy and recently immune checkpoints has considered as a novel treatment strategy to develop anti-cancer drugs. Many cancer types use the immune checkpoints and its ligand, PD-1/PD-L1 pathway, to evade detection and destruction by the immune system, which is associated with altered effector function of PD-1 and PD-L1 overexpression on cancer cells to deactivate T cells. In recent years, mAbs have been employed to block immune checkpoints, therefore normalization of the anti-tumor response has enabled the scientists to develop novel biopharmaceuticals. In vivo affinity maturation of antibodies in targeted therapy has sometimes failed, and current experimental methods cannot accommodate the accurate structural details of protein-protein interactions. Therefore, determining favorable binding sites on the protein surface for modulator design of these interactions is a major challenge. In this study, we used the in silico methods to identify favorable binding sites on the PD-1 and PD-L1 and to optimize mAb variants on a large scale. At first, all the binding areas on PD-1 and PD-L1 have been identified. Then, using the RosettaDesign protocol, thousands of antibodies have been generated for 11 different regions on PD-1 and PD-L1 and then the designs with higher stability, affinity, and shape complementarity were selected. Next, molecular dynamics simulations and MM-PBSA analysis were employed to understand the dynamic, structural features of the complexes and measure the binding affinity of the final designs. Our results suggest that binding sites 1, 3 and 6 on PD-1 and binding sites 9 and 11 on PD-L1 can be regarded as the most appropriate sites for the inhibition of PD-1-PD-L1 interaction by the designed antibodies. This study provides comprehensive information regarding the potential binding epitopes on PD-1 which could be considered as hotspots for designing potential biopharmaceuticals. We also showed that mutations in the CDRs regions will rearrange the interaction pattern between the designed antibodies and targets (PD-1 and PD-L1) with improved affinity to effectively inhibit protein-protein interaction and block the immune checkpoint.

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The Effects of Drug Addiction on the Brain and Body

Signs of drug addiction, effects of drug addiction.

Drug addiction is a treatable, chronic medical disease that involves complex interactions between a person’s environment, brain circuits, genetics, and life experiences.

People with drug addictions continue to use drugs compulsively, despite the negative effects.

Substance abuse has many potential consequences, including overdose and death. Learn about the effects of drug addiction on the mind and body and treatment options that can help.

Verywell / Theresa Chiechi

Drug Abuse vs. Drug Addiction

While the terms “drug abuse” and “drug addiction” are often used interchangeably, they're different. Someone who abuses drugs uses a substance too much, too frequently, or in otherwise unhealthy ways. However, they ultimately have control over their substance use.

Someone with a drug addiction uses drugs in a way that affects many parts of their life and causes major disruptions. They continue to use drugs compulsively despite the negative consequences.

The signs of drug abuse and addiction include changes in behavior, personality, and physical appearance. If you’re concerned about a loved one’s substance use, here are some of the red flags to watch out for:

Changes in school or work performance
Secretiveness
Relationship problems
Risk-taking behavior
Legal problems
Aggression
Mood swings
Changes in hobbies or friends
Sudden weight loss or gain
Unexplained odors on the body or clothing

Drug Addiction in Men and Women

Men and women are equally likely to develop drug addictions. However, men are more likely than women to use illicit drugs, die from a drug overdose, and visit an emergency room for addiction-related health reasons. Women are more susceptible to intense cravings and repeated relapses.

People can become addicted to any psychoactive ("mind-altering") substance. Common addictive substances include alcohol , tobacco ( nicotine ), stimulants, hallucinogens, and opioids .

Many of the effects of drug addiction are similar, no matter what substance someone uses. The following are some of the most common effects of drug addiction.

Effects of Drug Addiction on the Body

Drug addiction can lead to a variety of physical consequences ranging in seriousness from drowsiness to organ damage and death:

Shallow breathing
Elevated body temperature
Rapid heart rate
Increased blood pressure
Impaired coordination and slurred speech
Decreased or increased appetite
Tooth decay
Skin damage
Sexual dysfunction
Infertility
Kidney damage
Liver damage and cirrhosis
Various forms of cancer
Cardiovascular problems
Lung problems
Overdose and death

If left untreated drug addiction can lead to serious, life-altering effects on the body.

Dependence and withdrawal also affect the body:

Physical dependence : Refers to the reliance on a substance to function day to day. People can become physically dependent on a substance fairly quickly. Dependence does not always mean someone is addicted, but the longer someone uses drugs, the more likely their dependency is to become an addiction.
Withdrawal : When someone with a dependence stops using a drug, they can experience withdrawal symptoms like excessive sweating, tremors, panic, difficulty breathing, fatigue , irritability, and flu-like symptoms.

Overdose Deaths in the United States

According to the Centers for Disease Control and Prevention (CDC), over 100,000 people in the U.S. died from a drug overdose in 2021.

Effects of Drug Addiction on the Brain

All basic functions in the body are regulated by the brain. But, more than that, your brain is who you are. It controls how you interpret and respond to life experiences and the ways you behave as a result of undergoing those experiences.

Drugs alter important areas of the brain. When someone continues to use drugs, their health can deteriorate both psychologically and neurologically.

Some of the most common mental effects of drug addiction are:

Cognitive decline
Memory loss
Mood changes and paranoia
Poor self/impulse control
Disruption to areas of the brain controlling basic functions (heart rate, breathing, sleep, etc.)

Effects of Drug Addiction on Behavior

Psychoactive substances affect the parts of the brain that involve reward, pleasure, and risk. They produce a sense of euphoria and well-being by flooding the brain with dopamine .

This leads people to compulsively use drugs in search of another euphoric “high.” The consequences of these neurological changes can be either temporary or permanent.

Difficulty concentrating
Irritability
Angry outbursts
Lack of inhibition
Decreased pleasure/enjoyment in daily life (e.g., eating, socializing, and sex)
Hallucinations

Help Someone With Drug Addiction

If you suspect that a loved one is experiencing drug addiction, address your concerns honestly, non-confrontationally, and without judgment. Focus on building trust and maintaining an open line of communication while setting healthy boundaries to keep yourself and others safe. If you need help, contact the SAMHSA National Helpline at 1-800-662-4357.

Effects of Drug Addiction on an Unborn Child

Drug addiction during pregnancy can cause serious negative outcomes for both mother and child, including:

Preterm birth
Maternal mortality

Drug addiction during pregnancy can lead to neonatal abstinence syndrome (NAS) . Essentially, the baby goes into withdrawal after birth. Symptoms of NAS differ depending on which drug has been used but can include:

Excessive crying
Sleeping and feeding issues

Children exposed to drugs before birth may go on to develop issues with behavior, attention, and thinking. It's unclear whether prenatal drug exposure continues to affect behavior and the brain beyond adolescence.

While there is no single “cure” for drug addiction, there are ways to treat it. Treatment can help you control your addiction and stay drug-free. The primary methods of treating drug addiction include:

Psychotherapy : Psychotherapy, such as cognitive behavioral therapy (CBT) or family therapy , can help someone with a drug addiction develop healthier ways of thinking and behaving.
Behavioral therapy : Common behavioral therapies for drug addiction include motivational enhancement therapy (MET) and contingency management (CM). These therapy approaches build coping skills and provide positive reinforcement.
Medication : Certain prescribed medications help to ease withdrawal symptoms. Some examples are naltrexone (for alcohol), bupropion (for nicotine), and methadone (for opioids).
Hospitalization : Some people with drug addiction might need to be hospitalized to detox from a substance before beginning long-term treatment.
Support groups : Peer support and self-help groups, such as 12-step programs like Alcoholics Anonymous, can help people with drug addictions find support, resources, and accountability.

A combination of medication and behavioral therapy has been found to have the highest success rates in preventing relapse and promoting recovery. Forming an individualized treatment plan with your healthcare provider's help is likely to be the most effective approach.

Drug addiction is a complex, chronic medical disease that results in compulsive use of psychoactive substances despite the negative consequences.

Some effects of drug abuse and addiction include changes in appetite, mood, and sleep patterns. More serious health issues such as cognitive decline, major organ damage, overdose, and death are also risks. Addiction to drugs while pregnant can lead to serious outcomes for both mother and child.

Treatment for drug addiction may involve psychotherapy , medication, hospitalization, support groups, or a combination.

If you or someone you know is experiencing substance abuse or addiction, contact the Substance Abuse and Mental Health Services Administration (SAMHSA) National Helpline at 1-800-662-4357.

American Society of Addiction Medicine. Definition of addiction .

HelpGuide.org. Drug Abuse and Addiction .

Tennessee Department of Mental Health & Substance Abuse Services. Warning signs of drug abuse .

National Institute on Drug Abuse. Sex and gender differences in substance use .

Cleveland Clinic. Drug addiction .

National Institute on Drug Abuse. Drugs, Brains, and Behavior: The Science of Addiction Drugs and the Brain .

American Heart Association. Illegal Drugs and Heart Disease .

American Addiction Centers. Get the facts on substance abuse .

Szalavitz M, Rigg KK, Wakeman SE. Drug dependence is not addiction-and it matters . Ann Med . 2021;53(1):1989-1992. doi:10.1080/07853890.2021.1995623

Centers for Disease Control and Prevention. Drug overdose deaths in the U.S. top 100,000 annually .

American Psychological Association. Cognition is central to drug addiction .

National Institute on Drug Abuse. Understanding Drug Use and Addiction DrugFacts .

MedlinePlus. Neonatal abstinence syndrome .

National Institute on Drug Abuse. Treatment and recovery .

Grella CE, Stein JA. Remission from substance dependence: differences between individuals in a general population longitudinal survey who do and do not seek help . Drug and Alcohol Dependence. 2013;133(1):146-153. doi:10.1016/j.drugalcdep.2013.05.019

By Laura Dorwart Dr. Dorwart has a Ph.D. from UC San Diego and is a health journalist interested in mental health, pregnancy, and disability rights.

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Ecancermedicalscience

Innovative approaches for cancer treatment: current perspectives and new challenges

Carlotta pucci.

1 Smart Bio-Interfaces, Istituto Italiano di Tecnologia, 56025 Pisa, Italy

a https://orcid.org/0000-0002-8976-3711

Chiara Martinelli

b https://orcid.org/0000-0001-9360-1689

Gianni Ciofani

2 Department of Mechanical and Aerospace Engineering, Politecnico di Torino, 10129 Torino, Italy

c https://orcid.org/0000-0003-1192-3647

Every year, cancer is responsible for millions of deaths worldwide and, even though much progress has been achieved in medicine, there are still many issues that must be addressed in order to improve cancer therapy. For this reason, oncological research is putting a lot of effort towards finding new and efficient therapies which can alleviate critical side effects caused by conventional treatments. Different technologies are currently under evaluation in clinical trials or have been already introduced into clinical practice. While nanomedicine is contributing to the development of biocompatible materials both for diagnostic and therapeutic purposes, bioengineering of extracellular vesicles and cells derived from patients has allowed designing ad hoc systems and univocal targeting strategies. In this review, we will provide an in-depth analysis of the most innovative advances in basic and applied cancer research.

Introduction

Cancer is one of the main causes of death worldwide, and in the past decade, many research studies have focused on finding new therapies to reduce the side effects caused by conventional therapies.

During cancer progression, tumours become highly heterogeneous, creating a mixed population of cells characterised by different molecular features and diverse responsivity to therapies. This heterogeneity can be appreciated both at spatial and temporal levels and is the key factor responsible for the development of resistant phenotypes promoted by a selective pressure upon treatment administration [ 1 ]. Usually, cancer is treated as a global and homogeneous disease and tumours are considered as a whole population of cells. Thus, a deep understanding of these complex phenomena is of fundamental importance in order to design precise and efficient therapies.

Nanomedicine offers a versatile platform of biocompatible and biodegradable systems that are able to deliver conventional chemotherapeutic drugs in vivo , increasing their bioavailability and concentration around tumour tissues, and improving their release profile [ 2 ]. Nanoparticles can be exploited for different applications, ranging from diagnosis to therapy [ 2 ].

Recently, extracellular vesicles (EVs), responsible for cancer development, microenvironment modification and required for metastatic progression, have been widely investigated as efficient drug delivery vehicles [ 3 ].

Natural antioxidants and many phytochemicals have been recently introduced as anti-cancer adjuvant therapies due to their anti-proliferative and pro-apoptotic properties [ 4 , 5 ].

Targeted therapy is another branch of cancer therapy aiming at targeting a specific site, such as tumour vasculature or intracellular organelles, leaving the surroundings unaffected. This enormously increases the specificity of the treatment, reducing its drawbacks [ 6 ].

Another promising opportunity relies on gene therapy and expression of genes triggering apoptosis [ 7 ] and wild type tumour suppressors [ 8 ], or the targeted silencing mediated by siRNAs, currently under evaluation in many clinical trials worldwide [ 9 ].

Thermal ablation of tumours and magnetic hyperthermia are opening new opportunities for precision medicine, making the treatment localised in very narrow and precise areas. These methods could be a potential substitute for more invasive practices, such as surgery [ 10 , 11 ].

Furthermore, new fields such as radiomics and pathomics are contributing to the development of innovative approaches for collecting big amounts of data and elaborate new therapeutic strategies [ 12 , 13 ] and predict accurate responses, clinical outcome and cancer recurrence [ 14 – 16 ].

Taken all together, these strategies will be able to provide the best personalised therapies for cancer patients, highlighting the importance of combining multiple disciplines to get the best outcome.

In this review, we will provide a general overview of the most advanced basic and applied cancer therapies, as well as newly proposed methods that are currently under investigation at the research stage that should overcome the limitation of conventional therapies; different approaches to cancer diagnosis and therapy and their current status in the clinical context will be discussed, underlining their impact as innovative anti-cancer strategies.

Nanomedicine

Nanoparticles are small systems (1–1,000 nm in size) with peculiar physicochemical properties due to their size and high surface-to-volume ratio [ 17 ]. Biocompatible nanoparticles are used in cancer medicine to overcome some of the issues related to conventional therapies, such as the low specificity and bioavailability of drugs or contrast agents [ 2 ]. Therefore, encapsulation of the active agents in nanoparticles will increase their solubility/biocompatibility, their stability in bodily fluids and retention time in the tumour vasculature [ 18 – 20 ]. Furthermore, nanoparticles can be engineered to be extremely selective for a precise target [ 21 , 22 ] (see the “Targeted therapy and immunotherapy” section) and to release the drug in a controlled way by responding to a specific stimulus [ 18 , 23 – 25 ]. This is the case of ThermoDox, a liposomal formulation that can release doxorubicin as a response to an increment of temperature [ 26 ].

Inorganic nanoparticles are generally used as contrast agents for diagnosis purposes. Among them, quantum dots are small light-emitting semiconductor nanocrystals with peculiar electronic and optical properties, which make them highly fluorescent, resistant to photobleaching and sensitive for detection and imaging purposes [ 27 ]. Combined with active ingredients, they can be promising tools for theranostic applications [ 27 ]. In a recent study, quantum dots coated with poly(ethylene glycol) (PEG) were conjugated to anti-HER2 antibody and localised in specific tumour cells [ 28 ].

Superparamagnetic iron oxide nanoparticles (SPIONs) are usually exploited as contrast agents in magnetic resonance imaging (MRI) because they interact with magnetic fields [ 29 , 30 ]. Five types of SPIONs have been tested for MRI: ferumoxides (Feridex in the US, Endorem in Europe), ferucarbotran (Resovist), ferucarbotran C (Supravist, SHU 555 C), ferumoxtran-10 (Combidex) and NC100150 (Clariscan). Ferucarbotran is currently available in few countries, while the others have been removed from the market [ 25 ]. SPIONs have also been studied for cancer treatment by magnetic hyperthermia (see the “Thermal ablation and magnetic hyperthermia” section), and a formulation of iron oxide coated with aminosilane called Nanotherm has been already approved for the treatment of glioblastoma [ 31 ].

Gold nanoparticles have raised interest because of their optical and electrical properties and low toxicity [ 32 – 34 ]. They are mainly used as contrast agents for X-ray imaging, computed tomography [ 25 ], photoacoustic imaging [ 35 ] and photodynamic therapy [ 36 ]. A nanoshell made of a silica core and a gold shell coated with PEG was approved by the Food and Drug Administration (FDA) in 2012 and commercialised as AuroShell (Nanospectra) for the treatment of breast cancer by photodynamic therapy [ 25 ].

Organic nanoparticles are mainly used as delivery systems for drugs. Liposomes and micelles are both made of phospholipids, but they differ in their morphology. Liposomes are spherical particles having at least one lipid bilayer, resembling the structure of cell membranes. They are mainly used to encapsulate hydrophilic drugs in their aqueous core, but hydrophobic drugs can also be accommodated in the bilayer or chemically attached to the particles [ 37 ]. Micelles, instead, own a hydrophobic core that can encapsulate hydrophobic drugs [ 38 ]. Doxil, doxorubicin-loaded PEGylated liposomes, were the first nanoparticles approved by the FDA in 1995 to treat AIDS-associated Kaposi’s sarcoma [ 39 ]. This formulation drastically reduces doxorubicin side effects. Since then, other liposomal formulations have been approved by the FDA for cancer therapy, such as Myocet and DaunoXome [ 40 – 42 ]. Polymeric nanoparticles are made of biocompatible or natural polymers, such as poly(lactide-co-glycolide), poly(ε-caprolactone), chitosan, alginate and albumin [ 43 ]. Some formulations have already been accepted by the FDA, such as Abraxane (albumin-paclitaxel particles for the treatment of metastatic breast cancer and pancreatic ductal adenocarcinoma) and Ontak (an engineered protein combining interleukin-2 and diphtheria toxins for the treatment of non-Hodgkin’s peripheral T-cell lymphomas).

As well as these systems, which have been either accepted or are under clinical investigation, it is worth mentioning some new nanoparticles currently undergoing testing at the research level, which should improve treatment performance. For example, solid lipid nanoparticles, made of lipids that are solid at body temperature [ 44 ], and fabricated to load hydrophobic drugs [ 45 ] have been demonstrated to give a higher drug stability and prolonged release compared to other systems; however, the encapsulation efficiency is often low because of their high crystallinity [ 46 ]. To overcome this issue, one or more lipids, liquid at room temperature (like oleic acid, for example), are included in the formulation [ 47 ]. Lipid nanoparticles are good candidates for brain tumour therapy as they are able to cross the blood–brain barrier (BBB) [ 48 ]. A recent work showed that lipid nanoparticles loaded with SPIONs and temozolomide are efficient to treat glioblastoma since they combine the effect of the conventional chemotherapy and hyperthermia [ 49 , 50 ]. Dendrimers are another family of nanoparticles composed of polymers with a repetitive branched structure and characterised by a globular morphology [ 51 , 52 ]. Their architecture can be easily controlled, making their structure extremely versatile for many applications. For example, some recent studies show that poly-L-lysine (PLL) dendrimers loaded with doxorubicin induce anti-angiogenic responses in in vivo tumour models [ 53 ]. Currently, there is only one clinical trial for a formulation named ImDendrim based on a dendrimer and on a rhenium complex coupled to an imidazolium ligand, for the treatment of inoperable liver cancers that do not respond to conventional therapies [ 54 ].

Extracellular vesicles for cancer diagnosis and therapy

EVs are classified in two categories based on their biogenesis. Specifically, exosomes are small vesicles of around 30–150 nm originated from endosomes in physiological and pathological conditions and released by a fusion of multivesicular bodies (MVBs) to the cell membrane [ 55 , 56 ], while shed microvesicles (sMVs), with a typical size of 50–1,300 nm, are present in almost any extracellular bodily fluid and are responsible for the exchange of molecular materials between cells [ 57 , 58 ]. Exosomes are involved in cancer development and spreading [ 3 , 59 , 60 ], in the bidirectional communication between tumour cells and surrounding tissues, and in the construction of the microenvironment needed for pre-metastatic niche establishment and metastatic progression [ 61 ]. Hence, circulating vesicles are clinically relevant in cancer diagnosis, prognosis and follow up. Exosomes are actually recognised as valid diagnostic tools, but they can also be isolated and exploited as anti-cancer vaccines or nanosized drug carriers in cancer therapy [ 62 ].

Nowadays, one of the main issues in cancer diagnosis is the early identification of biomarkers by non-invasive techniques. Obtaining a significant amount of information, before and during tumour treatment, should allow the monitoring of cancer progression and the efficacy of therapeutic regimens. Liquid biopsies to detect circulating tumour cells, RNAs, DNAs and exosomes have been used as indicators for personalised medicine [ 63 ]. In recent years, exosomes detection has been validated as a reliable tool for preclinical practice in different cancer types [ 64 ], thanks to the identification of their content: double-stranded DNA (dsDNA) [ 65 , 66 ], messenger RNA (mRNA), micro RNA (miRNA), long non-coding RNA (lncRNA) [ 67 ], proteins and lipids [ 68 ]. DsDNA has been detected in exosomes isolated from plasma and serum of different cancer cell types, and mutated genes involved in tumorigenesis, such as mutated KRAS and TP53 [ 69 , 70 ], have been identified as disease predictors. Similarly, exosomal AR-V7 mRNA has been used as a prognostic marker of resistance to hormonal therapy in metastatic prostate cancer patients [ 71 ]. Gene expression profiling of multiple RNAs from urinary exosomes has been adopted as an efficient diagnostic tool [ 72 ]. LncRNAs isolated from serum exosomes have been exploited for disease prognosis in colorectal cancer patients [ 73 ], and multiple miRNAs allow one to distinguish between different lung cancer subtypes [ 74 ]. GPC1-positive exosomes have been employed to detect pancreatic cancer [ 75 ], while circulating exosomal macrophage migration inhibitory factor (MIF) was able to predict liver metastasis onset [ 76 ]. Finally, multiple lipids present in urinary exosomes have been approved as prostate cancer indicators [ 77 ]. Due to the high variability of patient classes and sample size, and in order to obtain clinically significant results for a fast and effective diagnosis, huge investments in exosome research will be required in the near future.

Exosomes could also be exploited as natural, biocompatible and low immunogenic nanocarriers for drug delivery in cancer therapy. They can be passively loaded by mixing purified vesicles with small drugs [ 78 – 82 ], or actively loaded by means of laboratory techniques, such as electroporation and sonication [ 83 , 84 ]. Superparamagnetic nanoparticles conjugated to transferrin have been tested for the isolation of exosomes expressing transferrin receptor from mice blood. After incubation with doxorubicin, they have been used to target liver cancer cells in response to external magnetic fields, inhibiting cell growth both in vitro and in vivo [ 80 ]. Kim et al. [ 83 ] engineered mouse macrophage-derived exosomes with aminoethyl anisamide-PEG to target sigma receptor, overexpressed in lung cancer cells and passively loaded them with paclitaxel. These systems acted as targeting agents able to suppress metastatic growth in vivo .

Three clinical trials with loaded exosomes are currently ongoing for the treatment of different tumours [ 85 – 87 ]: a phase I trial is evaluating the ability of exosomes to deliver curcumin to normal and colon cancer tissues [ 85 ]; a phase II trial is investigating the in vivo performance of autologous tumour cell-derived microparticles carrying methotrexate in lung cancer patients [ 86 ] and a clinical inquiry is focusing on autologous erythrocyte-derived microparticles loaded with methotrexate for gastric, colorectal and ovarian cancer treatment [ 87 ].

Recently, new strategies to produce ad hoc exosomes have been developed. Cells releasing exosomes have been genetically engineered to overexpress specific macromolecules, or modified to release exosomes with particular targeting molecules [ 88 – 90 ].

Exosomes derived from different cancer cells have already been exploited as cancer vaccines. Autologous dendritic cell-derived exosomes with improved immunostimulatory function have been tested in a phase II clinical trial for the activation of CD8 + T cells [ 91 ] in non-small cell lung cancer (NSCLC) patients, observing disease stabilisation and a better overall survival [ 92 ]. In a phase I trial, ascites-derived exosomes supplemented with granulocyte-macrophage colony stimulating factor (GM-CSF) have been administered to colorectal cancer patients, soliciting a tumour-specific immune response [ 93 ].

Many issues related to exosomes clinical translation remain open and are mostly connected to the definition of preclinical procedures for isolation, quantification, storage and standard protocols for drug loading. It is becoming even more necessary to distinguish between tumour and healthy blood cell-derived vesicles to characterise their post-isolation half-life and to perform standard content analyses. For these purposes, innovative approaches and technologies have been set up, such as microarrays and specific monoclonal antibodies and RNA markers amplification strategies [ 94 ].

Natural antioxidants in cancer therapy

Every day, the human body undergoes several exogenous insults, such as ultraviolet (UV) rays, air pollution and tobacco smoke, which result in the production of reactive species, especially oxidants and free radicals, responsible for the onset of many diseases, including cancer. These molecules can also be produced as a consequence of clinical administration of drugs, but they are also naturally created inside our cells and tissues by mitochondria and peroxisomes, and from macrophages metabolism, during normal physiological aerobic processes.

Oxidative stress and radical oxygen species are able to damage DNA (genetic alterations, DNA double strand breaks and chromosomal aberrations [ 95 , 96 ]) and other bio-macromolecules [ 97 ], such as lipids (membrane peroxidation and necrosis [ 98 ]) and proteins (significantly changing the regulation of transcription factors and, as a consequence, of essential metabolic pathways [ 99 ]).

The protective mechanisms our body has developed against these molecules are sometimes insufficient to counteract the huge damages produced. Recently, in addition to research into the roles of the physiological enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GP), natural antioxidants such as vitamins, polyphenols and plant-derived bioactive compounds are being studied in order to introduce them as preventive agents and potential therapeutic drugs [ 100 , 101 ]. These molecules have anti-inflammatory and anti-oxidant properties and are found in many vegetables and spices [ 102 ]. Vitamins, alkaloids, flavonoids, carotenoids, curcumin, berberine, quercetin and many other compounds have been screened in vitro and tested in vivo , displaying appreciable anti-proliferative and pro-apoptotic properties, and have been introduced as complementary therapies for cancer [ 4 , 5 , 103 ].

Despite the advantages of using natural drugs, their translation into clinical practice remains difficult due to their limited bioavailability and/or toxicity. Curcumin, a polyphenolic compound extracted from turmeric ( Curcuma longa ), is a traditional Southeast Asian remedy with anti-inflammatory, anti-oxidant and chemopreventive and therapeutic activities [ 104 ]. It has been shown to have cytotoxic effects in different kinds of tumours, such as brain, lung, leukaemia, pancreatic and hepatocellular carcinoma [ 105 , 106 ], with no adverse effects in normal cells at the effective therapeutic doses [ 107 ]. Curcumin can modulate a plethora of cellular mechanisms [ 108 , 109 ]; however, its biological properties, and as a consequence, the treatment duration and the efficient therapeutic doses, have not been completely elucidated yet. This molecule is highly lipophilic, poorly soluble in water and not very stable [ 110 ]. Different strategies and specific carriers, such as liposomes and micelles [ 111 , 112 ], have been developed to improve its bioavailability. Currently, 24 clinical trials involving curcumin are ongoing and 23 have been already completed [ 113 ].

Berberine is an alkaloid compound extracted from different plants, such as Berberis . Recently, it has been demonstrated to be effective against different tumours and to act as a chemopreventive agent, modulating many signalling pathways [ 114 , 115 ]. Like curcumin, it is poorly soluble in water; therefore, different nanotechnological strategies have been developed to facilitate its delivery across cell membranes [ 116 – 119 ]; six clinical trials are open and one has been completed [ 120 ].

Quercetin, a polyphenolic flavonoid found in fruits and vegetable, has been proven to be effective to treat several tumours, such as lung, prostate, liver, colon and breast cancers [ 121 – 123 ], by binding cellular receptors and interfering with many signalling pathways [ 124 ]. Interestingly, it has been shown to be effective also in combination with chemotherapeutic agents [ 125 ]. Presently, seven clinical trials are open and four have been completed [ 126 ].

Targeted therapy and immunotherapy

One of the main problems of conventional cancer therapy is the low specificity of chemotherapeutic drugs for cancer cells. In fact, most drugs act both on healthy and diseased tissues, generating severe side effects. Researchers are putting a lot of effort into finding a way to target only the desired site. Nanoparticles have raised great interest for their tendency to accumulate more in tumour tissues due to the enhanced permeability and retention effect (EPR) [ 127 ]. This process, called passive targeting, relies on the small size of nanoparticles and the leaky vasculature and impaired lymphatic drainage of neoplastic tissues [ 6 ]. Passive targeting, however, is difficult to control and can induce multidrug resistance (MDR) [ 128 ]. Active targeting, on the other hand, enhances the uptake by tumour cells by targeting specific receptors that are overexpressed on them [ 129 , 130 ]. Nanoparticles, for example, can be functionalized with ligands that univocally bind particular cells or subcellular sites [ 6 ]. Several kinds of ligands can be used, such as small molecules, peptides, proteins, aptamers and antibodies.

Folic acid and biotin are small molecules, whose receptors are overexpressed in tumour tissues. Several nanocarriers have been functionalized with folic acid to target ovarian and endometrial cancers [ 131 ]: folic acid-conjugated polyethylene glycol-poly(lactic-co-glycolic acid) nanoparticles delivering docetaxel increased drug cellular uptake by human cervical carcinoma cells [ 132 ]. Small ligands are cheap and can be linked to nanoparticles by simple conjugation chemistry [ 133 , 134 ].

Different kinds of small peptides and proteins are also effective in active targeting. Angiopep-2 is a peptide that has raised great interest in the treatment of brain cancer [ 135 ], because it binds to low-density lipoprotein receptor-related protein-1 (LRP1) of endothelial cells in the BBB, and it is also overexpressed in glioblastoma cancer cells [ 136 ]. Bombesin peptide conjugated to poly(lactic-co-glycolic acid) (PLGA) nanoparticles loaded with docetaxel was used to target the gastrin-releasing peptide receptor, overexpressed on cell surface of prostate, breast, ovarian, pancreatic and colorectal cancer cells [ 137 , 138 ]. Transferrin is a serum glycoprotein overexpressed on many solid tumours, especially on glioblastoma multiforme cells [ 139 ], and on epithelial cells of the BBB [ 6 , 140 ]. Transferrin-conjugated chitosan-PEG nanoparticles delivering paclitaxel exhibited a higher cytotoxicity towards transferrin-overexpressing human non-small cell lung cancer cells (NSCLCs) (HOP-62) [ 141 ].

Aptamers are small synthetic single-stranded RNA or DNA oligonucleotides folded into specific shapes that make them capable of binding specific targets [ 142 ]. Farokhzad et al. [ 143 ] reported that the use of A10 RNA aptamer conjugated to docetaxel-loaded nanoparticles significantly enhances in vitro cytotoxicity. The same aptamer has been also used to prepare quantum dot-doxorubicin conjugates [ 144 ].

Antibodies are currently the most exploited ligands for active targeting. These proteins have a typical ‘Y’ shape, where the two arms are responsible for the selective interaction with the antigen [ 145 ]. Antibodies can be used as immunoconjugates, when conjugated to a drug or nanoparticle, or naked. In the first case, their function is mainly to target a specific antigen overexpressed on cancer cells. Antibodies used for this purpose include those ones that bind to the human epidermal growth factor receptor 2 (HER2), the epidermal growth factor receptor (EGFR), the transferrin receptor (TfR) and the prostate-specific membrane antigen (PSMA) [ 6 ]. Rapamycin-PLGA nanoparticle conjugated to EGFR antibody exhibited higher cellular uptake by human breast adenocarcinoma cells (MCF-7), with enhanced apoptotic activity [ 146 ]. Loperamide-loaded human serum albumin nanoparticles conjugated to antibodies that specifically bind transferrin receptor successfully crossed the BBB and delivered the drug to the desired site [ 147 ].

Naked antibodies or immunoconjugates can also be used in immunotherapy, which is a cancer treatment that aims at stimulating or restoring the immune system of the patient against cancer cells [ 148 ]. Antibodies can act as markers for cancer cells to make them more vulnerable to the immune system response (non-specific immune stimulation), or as inhibitors for immune checkpoint proteins on cancer cell surface, that can modulate the action of T-cells [ 148 ]. Several antibodies have been already tested and accepted by FDA for immunotherapy, such as rituximab (1997, [ 149 ]), ibritumomab tiuxetan (2002, [ 150 ]), trastuzumab emtansine (2013, [ 151 ]), nivolumab (2014, [ 152 ]) and pembrolizumab (2014, [ 153 ]).

Immunotherapy can be achieved by another strategy called adoptive cell transfer (ACT) and it consists of isolating T-lymphocytes (T-cells) with the highest activity against cancer directly from the patient’s blood, expanding them ex vivo , and reinfusing them again into the patient [ 154 ]. Autologous T-cells can be genetically engineered in vitro to express a chimaeric antigen receptor (CAR), which makes them more specific against cancer cell antigens [ 148 ]. Different CARs can be designed to be directed against a certain cancer antigen. The genetic modification of T-cells can be achieved by different methods such as viral transduction, non-viral methods like DNA-based transposons, CRISPR/Cas9 or other plasmid DNA and mRNA transfer techniques (i.e., electroporation, encapsulation in nanoparticles) [ 155 ]. ACT protocols have been already adopted in clinical practice for advanced or recurrent acute lymphoblastic leukaemia and for some aggressive forms of non-Hodgkin’s lymphoma [ 148 ]. For example, it has been shown that the treatment of end-stage patients affected by acute lymphocytic leukaemia with CAR T-cells led to a full recovery in up to 92% of patients [ 155 ]. Despite these very promising results, much research is currently devoted to understanding the long-term side effects of CAR T-cell therapies and their fate within tumours, and to improving CAR T-cell expansion technologies.

Gene therapy for cancer treatment

Gene therapy is intended as the introduction of a normal copy of a defective gene in the genome in order to cure specific diseases [ 156 ]. The first application dates back to 1990 when a retroviral vector was exploited to deliver the adenosine deaminase (ADA) gene to T-cells in patients with severe combined immunodeficiency (SCID) [ 157 ]. Further research demonstrated that gene therapy could be applied in many human rare and chronic disorders and, most importantly, in cancer treatment. Approximately 2,900 gene therapy clinical trials are currently ongoing, 66.6% of which are related to cancer [ 158 ]. Different strategies are under evaluation for cancer gene therapy: 1) expression of pro-apoptotic [ 159 , 160 ] and chemo-sensitising genes [ 4 ]; 2) expression of wild type tumour suppressor genes [ 5 ]; 3) expression of genes able to solicit specific antitumour immune responses and 4) targeted silencing of oncogenes.

One approach relied on thymidine kinase (TK) gene delivery, followed by administration of prodrug ganciclovir to activate its expression and induce specific cytotoxicity [ 161 ]. This has been clinically translated for the treatment of prostate cancer and glioma [ 162 – 164 ]. In recent decades, different vectors carrying the p53 tumour suppressor gene have been evaluated for clinical applications. ONYX-015 has been tested in NSCLC patients and gave a high response rate when administered alone or together with chemotherapy [ 165 ]. Gendicine, a recombinant adenovirus carrying wild-type p53 in head and neck squamous cell cancer had a similar success, inducing complete disease regression when combined with radiotherapy [ 166 ].

Despite many achievements, there are still some challenges to face when dealing with gene therapy, such as the selection of the right conditions for optimal expression levels and the choice of the best delivery system to univocally target cancer cells. Gene therapy also presents some drawbacks linked to genome integration, limited efficacy in specific subsets of patients and high chances of being neutralised by the immune system. Therefore, particular interest has been elicited by targeted gene silencing approaches.

RNA interference (RNAi) has been recently established as an efficient technology both for basic research and medical translation. Small interfering RNAs (siRNAs) consist of double-stranded RNAs [ 167 ] able to produce targeted gene silencing. This process is intracellularly mediated by the RNA-induced silencing complex (RISC), responsible for cleaving the messenger RNA (mRNA), thus leading to interference with protein synthesis [ 168 ]. This physiological mechanism has been demonstrated in many eukaryotes, including animals. A few years after RNAi discovery, the first clinical application for wet-age related macular degeneration treatment entered phase I clinical trial [ 169 ]. Since cancer is triggered by precise molecular mechanisms, siRNAs can be rationally designed to block desired targets responsible for cell proliferation and metastatic invasion. This strategy relies on siRNA-mediated gene silencing of anti-apoptotic proteins [ 170 ], transcription factors (i.e., c-myc gene) [ 171 , 172 ] or cancer mutated genes (i.e., K-RAS ) [ 173 ]. Most of the clinical trials currently ongoing are based on local administration of siRNA oligonucleotides in a specific tissue/organ or on systemic delivery throughout the entire body [ 9 , 174 ]. Using siRNA-based drugs has several advantages: 1) safety, since they do not interact with the genome; 2) high efficacy, because only small amounts can produce a dramatic gene downregulation; 3) possibility of being designed for any specific target; 4) fewer side effects when compared to conventional therapies and 5) low costs of production [ 175 , 176 ]. However, siRNAs are relatively unstable in vivo and can be phagocytosed during blood circulation, excreted by renal filtration, or undergo enzymatic degradation [ 177 ]. Occasionally, they can induce off-target effects [ 178 ] or elicit innate immune responses, followed by specific inflammation [ 179 , 180 ]. Since naked siRNAs are negatively charged hydrophilic molecules, they cannot spontaneously cross cell membranes. Consequently, different delivery strategies are currently under study, such as chemical modification, encapsulation into lipid or polymeric carriers or conjugation with organic molecules (polymers, peptides, lipids, antibodies, small molecules [ 181 ], for efficient targeting [ 182 , 183 ]). Chemical modifications include the insertion of a phosphorothioate at 3’ end to reduce exonuclease degradation [ 184 ], the introduction of 2’ O-methyl group to obtain longer half-life in plasma [ 185 ] and the modification by 2,4-dinitrophenol to favour membrane permeability [ 186 ]. Nevertheless, the degradation of modified siRNAs often elicits cytotoxic effects; therefore, it is preferable to design ad hoc nanocarriers.

Different cationic lipid nanoparticles, such as liposomes, micelles and solid lipid nanoparticles [ 183 ], have been exploited for siRNA loading. Cationic liposomes interact with negatively charged nucleic acids, which can be easily transfected by simple electrostatic interactions [ 187 , 188 ]. They can be constituted by 1,2-dioleoyl-3-trimethylammonium propane (DOTAP) and N-{1-(2,3-dioleoyloxy) propyl]-N,N,N-trimethylammonium methyl sulphate (DOTMA) [ 189 ]. A theranostic agent consisting of an anticancer survivin siRNA entrapped in PEGylated liposomes has been developed to achieve simultaneous localisation inside tumour cells by means of entrapped MR agents and fluorophores and reduction of proliferation in vivo [ 190 ].

Neutral liposomes based on 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) have shown high efficacy in mice models of ovarian carcinoma and colorectal cancer [ 191 , 192 ]. A phase I clinical trial is currently recruiting patients for evaluating the safety of siRNA-EphA2-DOPC when administered to patients with advanced and recurrent cancer [ 193 ].

Stable nucleic acid lipid particles (SNALPs) have been evaluated in non-human primates [ 194 ]. SiRNAs have been encapsulated in a mixture of cationic lipids coated with a shell of polyethylene glycol (PEG) [ 195 ]. SNALPs entered a phase I clinical trial in patients affected by advanced solid tumours with liver involvement [ 196 ] and a phase I/II trial for treating neuroendocrine tumours and adrenocortical carcinoma patients refractory to standard therapy [ 197 ].

SiRNAs can be condensed in cationic polymers such as chitosan, cyclodextrin and polyethylenimine (PEI). Chitosan is a natural polysaccharide that, due to its cationic charge, has been exploited as carrier for nucleic acids in vitro and in vivo [ 198 ]. Specifically, a targeted siRNA has been delivered in mice xenografts of breast cancer [ 199 ]. Cyclodextrin polymers coated with PEG, conjugated with human transferrin and carrying a siRNA called CALAA-01, inhibit tumour growth by reducing the expression of M2 subunit of ribonucleotide reductase (R2), and have entered a phase I clinical trial [ 200 ]. PEI is able to form small cationic nanoparticles containing siRNAs and it has been exploited as antitumoural, upon loading with HER-2 receptor-specific siRNA [ 201 ]. A phase II clinical trial is presently starting to evaluate siG12D LODER directed to mutated KRAS oncogene and encapsulated into a biodegradable polymeric matrix for locally treating advanced pancreatic cancer patients in combination with chemotherapy [ 202 ].

SiRNAs may be conjugated to peptides, antibodies and aptamers in order to improve their stability during circulation and to enhance cellular uptake [ 203 ]. A success is represented by siRNAs targeting PSMA, overexpressed in this type of cancer [ 204 ].

The introduction of nanocarriers has largely improved siRNAs stability, pharmacokinetics and biodistribution properties, and the targeting specificity [ 205 , 206 ]. Smart nanomaterials responsive to external (i.e., magnetic field, ultrasounds) and tumour-specific stimuli (i.e., acidic pH, redox conditions) are currently under the development for controlled release and reduction of undesired negative effects [ 207 , 208 ]. Nanocarriers delivering siRNAs undergo a series of pH variations from blood circulation to intracellular environment and, for this reason, many pH responsive materials have been designed to favour cargo release under specific pH conditions [ 209 ]. Poly(allylamine) phosphate nanocarriers, stable at physiological pH, have been developed to release siRNAs in the cytoplasm after disassembly at low endosomal pH [ 210 ].

Although there have been many successes, some questions remain open and make the clinical translation of the siRNA-based approach very challenging, such as the correct doses to be delivered to patients and the many variabilities observed between individuals and different stages of disease. Further research towards controlled release to reach only specific targets, and the set-up of the best personalised therapy for cancer patients will be necessary in the near future.

Thermal ablation and magnetic hyperthermia

Thermal ablation of tumours includes a series of techniques that exploit heat (hyperthermia) or cold (hypothermia) to destroy neoplastic tissues [ 13 ]. It is known that cell necrosis occurs at temperatures lower than -40°C or higher than 60°C. Long exposures to temperatures between 41°C and 55°C are also effective for tumour cell damage. Moreover, it has been shown that cancer cells are more sensitive to high temperatures than healthy ones [ 211 ].

Hypothermic ablation is due to the formation of ice crystals upon cooling, which destroy cell membranes and finally kill cells. Argon gas is the preferred cooling agent because it can cool down the surrounding tissues to -160°C. Also, gases at their critical point, such as nitrogen, can be exploited since they have a higher heat capacity than argon. However, the technology to control and direct them is not well developed yet [ 10 ].

Hyperthermic ablation currently comprises radiofrequency (RF), microwave and laser ablation [ 10 ].

RF ablation is the most used in clinics, because it is effective and safe [ 212 ]. An alternated current of RF waves is applied to a target zone by an insulated electrode tip, while a second electrode, needed to close the circuit, is placed on the skin surface [ 10 ]. The interaction with the current causes the oscillation of ions in the extracellular fluid, which, in turns, produces heat. The more conductive the medium, the more effective the process. For this reason, RF ablation works very well in the liver and in other areas with a high content of water and ions, whereas it has a poor effect in lungs [ 10 ]. Moreover, the efficiency of the treatment decreases with the size of the lesion, giving the best results for areas not larger than 3 cm 2 [ 213 , 214 ].

Microwave ablation is based on the electromagnetic interaction between microwaves and the polar molecules in tissues, like water, that causes their oscillation and the consequent increase in temperature. Unlike the electrical current in RF ablation, microwaves can propagate through any kind of tissue [ 215 , 216 ], and this allows high temperatures to be reached in a short amount of time, to have a deeper penetration and to treat larger areas of tumours [ 217 ].

Laser therapy exploits the properties of laser beams of being very narrow and extremely focused at a specific wavelength. This makes the treatment very powerful and precise, thus a promising alternative to conventional surgery [ 218 ]. The absorption of the light emitted by the laser results in the heating and subsequent damage of the treated area [ 219 ]. Depending on the specific application, different kinds of lasers can be used. Neodymium:yttrium-aluminium-garnet (Nd:YAG) lasers (wavelength of 1064 nm) and diode lasers (wavelength of 800–900 nm) are used to treat internal organs, since they have a penetration depth up to 10 cm [ 218 ]. Conversely, CO 2 lasers (10,600 nm), with a penetration depth of 10 μm up to 1 mm maximum are used for superficial treatments. Laser therapy is receiving a lot of attention in research because of its advantages compared to other ablation techniques, such as a higher efficacy, safety and precision, and a shorter treatment session needed to achieve the same results [ 220 , 221 ]. Moreover, the fibres to transmit laser light are compatible with MRI, allowing for a precise measure of the temperature and the thermal dose [ 222 ]. However, there are still some limitations to overcome, such as the need of a very skilled operator to place the fibre in the correct position [ 218 ].

Finally, a new way to heat tumour tissues, currently under study, is through magnetic hyperthermia. This technique exploits superparamagnetic or ferromagnetic nanoparticles that can generate heat after stimulation with an alternating magnetic field. The most studied systems in nanomedicine are SPIONs [ 11 ]. The production of heat, in this case, is due to the alignment of magnetic domains in the particles when the magnetic field is applied, and the subsequent relaxation processes (Brownian and/or Neel relaxations) during which heat is released, when the magnetic field is removed and the magnetisation of the particles reverts to zero [ 223 ]. Magnetic hyperthermia can reach any area of the body and SPIONs can also act as MRI contrast agents to follow their correct localisation before the stimulation. The particles can be coated with biocompatible polymers and/or lipid and functionalized with specific ligands to impart targeting properties [ 224 ]. As already mentioned, until now, just a formulation of 15-nm iron oxide nanoparticles coated with aminosilane (Nanotherm) obtained approval for the treatment of glioblastoma [ 31 ]. SPIONs have also been successfully encapsulated in lipid nanocarriers together with a chemotherapeutic agent to combine chemotherapy and hyperthermia [ 49 , 50 ].

Recent innovations in cancer therapy: Radiomics and pathomics

Efficient cancer therapy currently relies on surgery and, in approximately 50% of patients, on radiotherapy, that can be delivered by using an external beam source or by inserting locally a radioactive source (in this case, the approach is named brachytherapy), thus obtaining focused irradiation. Currently, localisation of the beam is facilitated by image-guided radiotherapy (IGRT), where images of the patient are acquired during the treatment allowing the best amount of radiation to be set. Thanks to the introduction of intensity-modulated radiotherapy (IMRT), radiation fields of different intensities can be created, helping to reduce doses received by healthy tissues and thus limiting adverse side effects. Finally, by means of stereotactic ablative radiotherapy (SABR), it has become feasible to convey an ablative dose of radiation only to a small target volume, significantly reducing undesired toxicity [ 225 ].

Unfortunately, radioresistance can arise during treatment, lowering its efficacy. This has been linked to mitochondrial defects; thus, targeting specific functions have proven to be helpful in restoring anti-cancer effects [ 226 ]. A recent study has shown, for example, that radioresistance in an oesophageal adenocarcinoma model is linked to an abnormal structure and size of mitochondria, and the measurement of the energy metabolism in patients has allowed discrimination between treatment resistant and sensitive patients [ 227 ]. Targeting mitochondria with small molecules acting as radiosensitizers is being investigated for gastrointestinal cancer therapy [ 228 ].

Cancer is a complex disease and its successful treatment requires huge efforts in order to merge the plethora of information acquired during diagnostic and therapeutic procedures. The ability to link the data collected from medical images and molecular investigations has allowed an overview to be obtained of the whole tridimensional volume of the tumour by non-invasive imaging techniques. This matches with the main aim of precision medicine, which is to minimise therapy-related side effects, while optimising its efficacy to achieve the best individualised therapy [ 229 ].

Radiomics and pathomics are two promising and innovative fields based on accumulating quantitative image features from radiology and pathology screenings as therapeutic and prognostic indicators of disease outcome [ 12 , 13 , 230 ]. Many artificial intelligence technologies, such as machine learning application, have been introduced to manage and elaborate the massive amount of collected datasets and to accurately predict the treatment efficacy, the clinical outcome and the disease recurrence. Prediction of the treatment response can help in finding an ad hoc adaptation for the best prognosis and outcome. Nowadays, personalised medicine requires an integrated interpretation of the results obtained by multiple diagnostic approaches, and biomedical images are crucial to provide real-time monitoring of disease progression, being strictly correlated to cancer molecular characterisation.

Radiomics is intended as the high throughput quantification of tumour properties obtained from the analysis of medical images [ 14 , 15 , 231 ]. Pathomics, on the other side, relies on generation and characterisation of high-resolution tissue images [ 16 , 232 , 233 ]. Many studies are focusing on the development of new techniques for image analysis in order to extrapolate information by quantification and disease characterisation [ 234 , 235 ]. Flexible databases are required to manage big volumes of data coming from gene expression, histology, 3D tissue reconstruction (MRI) and metabolic features (positron emission tomography, PET) in order to identify disease phenotypes [ 236 , 237 ].

Currently, there is an urgent need to define univocal data acquisition guidelines. Some initiatives to establish standardised procedures and facilitate clinical translation have been already undertaken, such as quantitative imaging network [ 238 ] or the German National Cohort Consortium [ 239 ]. Precise description of the parameters required for image acquisition and for the creation and use of computational and statistical methods are necessary to set robust protocols for the generation of models in radiation therapy. According to the US National Library of Medicine, approximately 50 clinical trials involving radiomics are currently recruiting patients, and a few have already been completed [ 240 ].

Conclusions and future perspectives

In recent years, research into cancer medicine has taken remarkable steps towards more effective, precise and less invasive cancer treatments ( Figure 1 ). While nanomedicine, combined with targeted therapy, helped improving the biodistribution of new or already tested chemotherapeutic agents around the specific tissue to be treated, other strategies, such as gene therapy, siRNAs delivery, immunotherapy and antioxidant molecules, offer new possibilities to cancer patients. On the other hand, thermal ablation and magnetic hyperthermia are promising alternatives to tumour resection. Finally, radiomics and pathomics approaches help the management of big data sets from cancer patients to improve prognosis and outcome.

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At the moment, the most frequent entries concerning cancer therapies in the database of clinical trials ( www.clinicaltrials.gov ) involve the terms targeted therapy, immunotherapy and gene therapy, highlighting that these are the most popular methodologies under investigation, especially because, as already mentioned before, they have been shown to be very promising and effective ( Figure 2A ). However, Figure 2B shows that the clinical trials started in the past decade on different therapies mentioned in this review (except for liposomes-based therapies) have increased in number, showing how the interest on these new approaches is quickly growing in order to replace and/or improve conventional therapies. In particular, radiomics, immunotherapy and exosomes are the entries whose number has increased the most in the last 10 years.

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The current scenario for cancer research is wide, offering many possibilities for the constant improvement of treatment, considering not only patient recovery but also caring for their well-being during therapy. As summarised in Table 1 , these new approaches offer many advantages compared to conventional therapies. However, some disadvantages still have to be overcome to improve their performances. Much progress has been made, but many others are likely to come in the near future, producing more and more ad hoc personalised therapies.

Strategy	Advantages	Disadvantages
Nanoparticles	• High stability and specificity • Good biocompatibility and bioavailability	• It depends on the particular nanoparticle
EVs	• Physiologically secreted • Good molecular characterisation • High biocompatibility • modifiable/loadable	• Lack of preclinical procedures for isolation, quantification, storage and drug loading
Natural antioxidants	• Easily available in large quantities • Exploitation of their intrinsic properties	• Limited bioavailability • Possible toxicity
Targeted therapy	• High specificity • Reduction of adverse reactions	• Lack of information regarding long-term side effects
Gene therapy	• Expression of pro-apoptotic and chemo-sensitising genes • Expression of wild type tumour suppressor genes • Expression of genes able to solicit specific anti-tumour immune responses • Targeted silencing of oncogenes and safety (RNAi)	• Genome integration • Limited efficacy in specific subsets of patients • High chances to be neutralised by immune system • Off-target effects and inflammation (RNAi) • Need of delivery systems (RNAi) • Set-up of doses and suitable conditions for controlled release (RNAi)
Thermal ablation Magnetic hyperthermia	• Precise treatment of the interested area • Possibility to perform the treatment along with MRI imaging (magnetic hyperthermia)	• High efficiency only for localised areas • Low penetration power • Need for a skilled operator to perform the treatment
Radiomics/pathomics	• Creation of tumour whole tridimensional volume by non-invasive imaging techniques • Therapeutic and prognostic indicators of disease outcome	• Definition of univocal data acquisition guidelines • Standardisation of procedures to facilitate clinical translation • Description of parameters and computational/statistical methods to set robust protocols for the generation of models for therapy

Conflicts of interest

The authors declare that they have no conflict of interest.

Funding declaration

This work was partially supported by the Fondazione CaRiPLo, grant no. 2018-0156 (Nanotechnological countermeasures against Oxidative stress in muscle cells Exposed to Microgravity—NOEMI) and by the European Research Council (ERC) under the European Union’s Horizon 2020 Research and Innovation Programme (grant agreement N°709613, SLaMM).

Authors’ contributions

Carlotta Pucci and Chiara Martinelli contributed equally to this work.

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Something’s Poisoning America’s Land. Farmers Fear ‘Forever’ Chemicals.

Fertilizer made from city sewage has been spread on millions of acres of farmland for decades. Scientists say it can contain high levels of the toxic substance.

Jordan Vonderhaar for The New York Times

Hiroko Tabuchi traveled to Texas and Michigan and interviewed ranchers, scientists, investigators and wastewater-treatment experts for this article.

Aug. 31, 2024

Supported by

For decades, farmers across America have been encouraged by the federal government to spread municipal sewage on millions of acres of farmland as fertilizer. It was rich in nutrients, and it helped keep the sludge out of landfills.

But a growing body of research shows that this black sludge, made from the sewage that flows from homes and factories, can contain heavy concentrations of chemicals thought to increase the risk of certain types of cancer and to cause birth defects and developmental delays in children.

Known as “forever chemicals” because of their longevity, these toxic contaminants are now being detected, sometimes at high levels, on farmland across the country , including in Texas, Maine, Michigan, New York and Tennessee. In some cases the chemicals are suspected of sickening or killing livestock and are turning up in produce. Farmers are beginning to fear for their own health.

The national scale of farmland contamination by these chemicals — which are used in everything from microwave popcorn bags and firefighting gear to nonstick pans and stain-resistant carpets — is only now starting to become apparent. There are now lawsuits against providers of the fertilizer, as well as against the Environmental Protection Agency, alleging that the agency failed to regulate the chemicals, known as PFAS.

In Michigan, among the first states to investigate the chemicals in sludge fertilizer, officials shut down one farm where tests found particularly high concentrations in the soil and in cattle that grazed on the land. This year, the state prohibited the property from ever again being used for agriculture. Michigan hasn’t conducted widespread testing at other farms, partly out of concern for the economic effects on its agriculture industry.

Interior of an empty barn, weeds peeking up through the floor.

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Yingying Tang 1 ,
Shijie Tang 2 ,
Wenjuan Yang 1 ,
Zhengyan Zhang 1 ,
Teng Wang 2 ,
Yuyun Wu 2 ,
Junyi Xu 1 ,
Christian Pilarsky 3 ,
Massimiliano Mazzone 4 , 5 ,
Lei-Wei Wang 6 ,
http://orcid.org/0000-0002-5937-634X Yongwei Sun 7 ,
Ruijun Tian 8 ,
Yujie Tang 9 ,
Yu Wang 6 ,
http://orcid.org/0000-0003-2346-2884 Chaochen Wang 2 , 10 , 11 ,
http://orcid.org/0000-0002-6497-1792 Jing Xue 1
1 State Key Laboratory of Systems Medicine for Cancer, Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine , Shanghai , China
2 Centre of Biomedical Systems and Informatics, ZJU-UoE Institute, Zhejiang University School of Medicine, International Campus, Zhejiang University, Haining , Zhejiang , China
3 Department of Surgery , Universitätsklinikum Erlangen, Friedrich-Alexander Universität Erlangen-Nürnberg (FAU) , Erlangen , Germany
4 Laboratory of Tumor Inflammation and Angiogenesis, Center for Cancer Biology, VIB, Leuven, Belgium , Leuven , Belgium
5 Laboratory of Tumor Inflammation and Angiogenesis, Center for Cancer Biology, Department of Oncology , Leuven , Belgium
6 Department of Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University , Shanghai , China
7 Department of Biliary and Pancreatic Surgery , Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital , Shanghai , China
8 Shenzhen Key Laboratory of Functional Proteomics, Guangming Advanced Research Institute, Southern University of Science and Technology , Shenzhen , China
9 Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Department of Histoembryology, Genetics and Developmental Biology, Shanghai Jiao Tong University School of Medicine , Shanghai , China
10 Department of Breast Surgery , The Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang University, Hangzhou , Hangzhou , China
11 Biomedical and Health Translational Research Centre, Zhejiang University , Zhejiang , China
Correspondence to Jing Xue, State Key Laboratory of Systems Medicine for Cancer, Stem Cell Research Center, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; xuejing0904{at}126.com ; Dr Chaochen Wang; chaochenwang{at}intl.zju.edu.cn ; Dr Yu Wang; wangyu4tc{at}163.com ; Dr Yujie Tang; yujietang{at}shsmu.edu.cn

Objective Pancreatic ductal adenocarcinoma (PDAC) stands as one of the most lethal cancers, marked by its lethality and limited treatment options, including the utilisation of checkpoint blockade (ICB) immunotherapy. Epigenetic dysregulation is a defining feature of tumourigenesis that is implicated in immune surveillance, but remains elusive in PDAC.

Design To identify the factors that modulate immune surveillance, we employed in vivo epigenetic-focused CRISPR-Cas9 screen in mouse PDAC tumour models engrafted in either immunocompetent or immunodeficient mice.

Results Here, we identified MED12 as a top hit, emerging as a potent negative modulator of immune tumour microenviroment (TME) in PDAC. Loss of Med12 significantly promoted infiltration and cytotoxicity of immune cells including CD8 + T cells, natural killer (NK) and NK1.1 + T cells in tumours, thereby heightening the sensitivity of ICB treatment in a mouse model of PDAC. Mechanistically, MED12 stabilised heterochromatin protein HP1A to repress H3K9me3-marked endogenous retroelements. The derepression of retrotransposons induced by MED12 loss triggered cytosolic nucleic acid sensing and subsequent activation of type I interferon pathways, ultimately leading to robust inflamed TME . Moreover, we uncovered a negative correlation between MED12 expression and immune resposne pathways, retrotransposon levels as well as the prognosis of patients with PDAC undergoing ICB therapy.

Conclusion In summary, our findings underscore the pivotal role of MED12 in remodelling immnue TME through the epigenetic silencing of retrotransposons, offering a potential therapeutic target for enhancing tumour immunogenicity and overcoming immunotherapy resistance in PDAC.

cancer immunobiology
cellular immunity
pancreatic cancer

Data availability statement

Data are available on reasonable request. All genomic sequencing data involved in this study have been deposited in the Gene Expression Omnibus database with the accession code GSE242098.

https://doi.org/10.1136/gutjnl-2024-332350

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YT, ST and WY contributed equally.

Contributors YYT and JX designed the experiments and interpreted the data; YYT and WJY performed most of the experiments; SJT, TW and YYW performed the bioinformatics analysis under the guidance of CCW; YW performed the retrospective study; ZYZ, and JYX, assisted in some experiments; YJT, YWS, LWW, RJT, MM and CP provided the key materials and assisted in some discussions; YYT and JX wrote the manuscript; JX and CCW provided overall guidance. Jing Xue acted as guarantor.

Funding This work was supported by the National Natural Science Foundation of China (no. 81970553, no. 81770628, no. 82022049, JXue), Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support (no. 20161312, JXue), the Innovative Research Team of High-Level Local Universities in Shanghai, 111 project (no. B21024, JXue).

Competing interests None declared.

Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

Provenance and peer review Not commissioned; externally peer reviewed.

Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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