a presentation about cancer

What Is Cancer?

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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

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.

• Patient Care & Health Information
• Diseases & Conditions

Cancer refers to any one of a large number of diseases characterized by the development of abnormal cells that divide uncontrollably and have the ability to infiltrate and destroy normal body tissue. Cancer often has the ability to spread throughout your body.

Cancer is the second-leading cause of death in the world. But survival rates are improving for many types of cancer, thanks to improvements in cancer screening, treatment and prevention.

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Signs and symptoms caused by cancer will vary depending on what part of the body is affected.

Some general signs and symptoms associated with, but not specific to, cancer, include:

• Lump or area of thickening that can be felt under the skin
• Weight changes, including unintended loss or gain
• Skin changes, such as yellowing, darkening or redness of the skin, sores that won't heal, or changes to existing moles
• Changes in bowel or bladder habits
• Persistent cough or trouble breathing
• Difficulty swallowing
• Persistent indigestion or discomfort after eating
• Persistent, unexplained muscle or joint pain
• Persistent, unexplained fevers or night sweats
• Unexplained bleeding or bruising

When to see a doctor

Make an appointment with your doctor if you have any persistent signs or symptoms that concern you.

If you don't have any signs or symptoms, but are worried about your risk of cancer, discuss your concerns with your doctor. Ask about which cancer screening tests and procedures are appropriate for you.

Cancer is caused by changes (mutations) to the DNA within cells. The DNA inside a cell is packaged into a large number of individual genes, each of which contains a set of instructions telling the cell what functions to perform, as well as how to grow and divide. Errors in the instructions can cause the cell to stop its normal function and may allow a cell to become cancerous.

What do gene mutations do?

A gene mutation can instruct a healthy cell to:

• Allow rapid growth. A gene mutation can tell a cell to grow and divide more rapidly. This creates many new cells that all have that same mutation.
• Fail to stop uncontrolled cell growth. Normal cells know when to stop growing so that you have just the right number of each type of cell. Cancer cells lose the controls (tumor suppressor genes) that tell them when to stop growing. A mutation in a tumor suppressor gene allows cancer cells to continue growing and accumulating.
• Make mistakes when repairing DNA errors. DNA repair genes look for errors in a cell's DNA and make corrections. A mutation in a DNA repair gene may mean that other errors aren't corrected, leading cells to become cancerous.

These mutations are the most common ones found in cancer. But many other gene mutations can contribute to causing cancer.

What causes gene mutations?

Gene mutations can occur for several reasons, for instance:

• Gene mutations you're born with. You may be born with a genetic mutation that you inherited from your parents. This type of mutation accounts for a small percentage of cancers.
• Gene mutations that occur after birth. Most gene mutations occur after you're born and aren't inherited. A number of forces can cause gene mutations, such as smoking, radiation, viruses, cancer-causing chemicals (carcinogens), obesity, hormones, chronic inflammation and a lack of exercise.

Gene mutations occur frequently during normal cell growth. However, cells contain a mechanism that recognizes when a mistake occurs and repairs the mistake. Occasionally, a mistake is missed. This could cause a cell to become cancerous.

How do gene mutations interact with each other?

The gene mutations you're born with and those that you acquire throughout your life work together to cause cancer.

For instance, if you've inherited a genetic mutation that predisposes you to cancer, that doesn't mean you're certain to get cancer. Instead, you may need one or more other gene mutations to cause cancer. Your inherited gene mutation could make you more likely than other people to develop cancer when exposed to a certain cancer-causing substance.

It's not clear just how many mutations must accumulate for cancer to form. It's likely that this varies among cancer types.

More Information

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Risk factors

While doctors have an idea of what may increase your risk of cancer, the majority of cancers occur in people who don't have any known risk factors. Factors known to increase your risk of cancer include:

Cancer can take decades to develop. That's why most people diagnosed with cancer are 65 or older. While it's more common in older adults, cancer isn't exclusively an adult disease — cancer can be diagnosed at any age.

Your habits

Certain lifestyle choices are known to increase your risk of cancer. Smoking, drinking more than one drink a day for women and up to two drinks a day for men, excessive exposure to the sun or frequent blistering sunburns, being obese, and having unsafe sex can contribute to cancer.

You can change these habits to lower your risk of cancer — though some habits are easier to change than others.

Your family history

Only a small portion of cancers are due to an inherited condition. If cancer is common in your family, it's possible that mutations are being passed from one generation to the next. You might be a candidate for genetic testing to see whether you have inherited mutations that might increase your risk of certain cancers. Keep in mind that having an inherited genetic mutation doesn't necessarily mean you'll get cancer.

Your health conditions

Some chronic health conditions, such as ulcerative colitis, can markedly increase your risk of developing certain cancers. Talk to your doctor about your risk.

Your environment

The environment around you may contain harmful chemicals that can increase your risk of cancer. Even if you don't smoke, you might inhale secondhand smoke if you go where people are smoking or if you live with someone who smokes. Chemicals in your home or workplace, such as asbestos and benzene, also are associated with an increased risk of cancer.

Complications

Cancer and its treatment can cause several complications, including:

• Pain. Pain can be caused by cancer or by cancer treatment, though not all cancer is painful. Medications and other approaches can effectively treat cancer-related pain.
• Fatigue. Fatigue in people with cancer has many causes, but it can often be managed. Fatigue associated with chemotherapy or radiation therapy treatments is common, but it's usually temporary.
• Difficulty breathing. Cancer or cancer treatment may cause a feeling of being short of breath. Treatments may bring relief.
• Nausea. Certain cancers and cancer treatments can cause nausea. Your doctor can sometimes predict if your treatment is likely to cause nausea. Medications and other treatments may help you prevent or decrease nausea.
• Diarrhea or constipation. Cancer and cancer treatment can affect your bowels and cause diarrhea or constipation.
• Weight loss. Cancer and cancer treatment may cause weight loss. Cancer steals food from normal cells and deprives them of nutrients. This is often not affected by how many calories or what kind of food is eaten; it's difficult to treat. In most cases, using artificial nutrition through tubes into the stomach or vein does not help change the weight loss.
• Chemical changes in your body. Cancer can upset the normal chemical balance in your body and increase your risk of serious complications. Signs and symptoms of chemical imbalances might include excessive thirst, frequent urination, constipation and confusion.
• Brain and nervous system problems. Cancer can press on nearby nerves and cause pain and loss of function of one part of your body. Cancer that involves the brain can cause headaches and stroke-like signs and symptoms, such as weakness on one side of your body.
• Unusual immune system reactions to cancer. In some cases the body's immune system may react to the presence of cancer by attacking healthy cells. Called paraneoplastic syndromes, these very rare reactions can lead to a variety of signs and symptoms, such as difficulty walking and seizures.
• Cancer that spreads. As cancer advances, it may spread (metastasize) to other parts of the body. Where cancer spreads depends on the type of cancer.
• Cancer that returns. Cancer survivors have a risk of cancer recurrence. Some cancers are more likely to recur than others. Ask your doctor about what you can do to reduce your risk of cancer recurrence. Your doctor may devise a follow-up care plan for you after treatment. This plan may include periodic scans and exams in the months and years after your treatment, to look for cancer recurrence.

Doctors have identified several ways to reduce your risk of cancer, such as:

• Stop smoking. If you smoke, quit. If you don't smoke, don't start. Smoking is linked to several types of cancer — not just lung cancer. Stopping now will reduce your risk of cancer in the future.
• Avoid excessive sun exposure. Harmful ultraviolet (UV) rays from the sun can increase your risk of skin cancer. Limit your sun exposure by staying in the shade, wearing protective clothing or applying sunscreen.
• Eat a healthy diet. Choose a diet rich in fruits and vegetables. Select whole grains and lean proteins. Limit your intake of processed meats.
• Exercise most days of the week. Regular exercise is linked to a lower risk of cancer. Aim for at least 30 minutes of exercise most days of the week. If you haven't been exercising regularly, start out slowly and work your way up to 30 minutes or longer.
• Maintain a healthy weight. Being overweight or obese may increase your risk of cancer. Work to achieve and maintain a healthy weight through a combination of a healthy diet and regular exercise.
• Drink alcohol in moderation, if you choose to drink. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.
• Schedule cancer screening exams. Talk to your doctor about what types of cancer screening exams are best for you based on your risk factors.
• Ask your doctor about immunizations. Certain viruses increase your risk of cancer. Immunizations may help prevent those viruses, including hepatitis B, which increases the risk of liver cancer, and human papillomavirus (HPV), which increases the risk of cervical cancer and other cancers. Ask your doctor whether immunization against these viruses is appropriate for you.

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What to know about cancer

Cancer causes cells to divide uncontrollably. This can result in tumors, damage to the immune system, and other impairment that can be fatal.

Cancer can affect various parts of the body, such as the breasts, lungs, prostate, and skin.

In this article, we examine types of cancer, how the disease develops, and how doctors may treat it. We also explore different types of cancer and disease outlook. Finally, we answer some common questions about cancer.

Cancer resources

To discover more evidence-based information and resources for cancer, visit our dedicated hub .

What is cancer?

Cancer is a broad term. It describes the disease that results when cellular changes cause the uncontrolled growth and division of cells .

Some types of cancer cause rapid cell growth, while others cause cells to grow and divide at a slower rate.

Certain forms of cancer result in visible growths called tumors , while others, such as leukemia , do not.

Most of the body’s cells have specific functions and fixed lifespans. Cell death is part of a natural and beneficial phenomenon, which healthcare professionals call apoptosis.

A cell receives instructions to die so that the body can replace it with a newer cell that functions better. Cancerous cells lack the components that instruct them to stop dividing and to die.

As a result, they build up in the body, using oxygen and nutrients that would usually nourish other cells. Cancerous cells can form tumors, impair the immune system and cause other changes that prevent the body from functioning regularly.

Cancerous cells may appear in one area, then spread via the lymph nodes . These are clusters of immune cells located throughout the body.

There are many causes of cancer, and some are preventable.

Risk factors

Preventable risk factors for cancer include :

• heavy alcohol consumption
• excess body weight
• physical inactivity
• poor nutrition
• human papillomavirus infection

Other risk factors for cancer are not preventable. Currently, the most significant unpreventable risk factor is age. According to the American Cancer Society (ACS), doctors in the United States diagnose 88% of cancer cases in people ages 50 years or older.

Is cancer genetic?

Genetic factors can contribute to the development of cancer.

A person’s genetic code tells their cells when to divide and expire. Changes in the genes can lead to faulty instructions, and cancer can result.

Genes also influence the cells’ production of proteins, and proteins carry many of the instructions for cellular growth and division.

Some genes change proteins that would usually repair damaged cells. This can lead to a predisposition for cancer. If a parent has these genes, they may pass on the altered instructions to their offspring. A doctor may refer to this as an inherited gene mutation. These mutations may contribute to the development of up to 10% of cancer cases.

Some genetic mutations that increase the risk of developing cancer occur after birth. Healthcare professionals refer to these changes as “acquired gene mutations”. Possible causes include smoking and sun exposure. These genetic changes cause cancer more commonly than inherited gene mutations.

Other changes that can result in cancer take place in the chemical signals that determine how the cells turn specific genes on and off. Doctors may call these “epigenetic changes”.

Doctors usually prescribe treatments based on the type of cancer, its stage at diagnosis, and the person’s overall health.

Some examples of cancer treatment include :

• Chemotherapy aims to kill cancerous cells with medications that target rapidly dividing cells. The drugs can also help shrink tumors, but the side effects can be severe.
• Hormone therapy involves taking medications that change how certain hormones work or interfere with the body’s ability to produce them. When hormones play a significant role, as with prostate and breast cancers , this is a common approach.
• Immunotherapy uses medications and other treatments to boost the immune system and encourage it to fight cancerous cells.
• Radiation therapy uses high-dose radiation to kill cancerous cells. Also, a doctor may recommend using radiation to shrink a tumor before surgery or reduce tumor-related symptoms.
• Stem cell transplant can be especially beneficial for people with blood-related cancers, such as leukemia or lymphoma . It involves removing cells, such as red or white blood cells , that chemotherapy or radiation has destroyed. Lab technicians then strengthen the cells and put them back into the body.
• Surgery is often a part of a treatment plan when a person has a cancerous tumor. Also, a surgeon may remove lymph nodes to reduce or prevent the disease’s spread.
• Targeted therapies perform functions within cancerous cells to prevent them from multiplying. They can also boost the immune system. Two examples of these therapies are small-molecule drugs and monoclonal antibodies.

Doctors will often employ more than one type of treatment to maximize effectiveness.

The most common type of cancer in the U.S. is breast cancer, followed by lung and prostate cancers, according to the National Cancer Institute, which excluded nonmelanoma skin cancers from these findings.

Each year, more than 40,000 people in the country receive a diagnosis of one of the following types of cancer:

• colon and rectal
• endometrial
• non-Hodgkin’s lymphoma

Other forms are less common. According to the National Cancer Institute, there are over 100 types of cancer.

Cancer development and cell division

Doctors classify cancer by its location in the body and the tissues that it forms in.

For example, sarcomas develop in bones or soft tissues, while carcinomas form in cells that cover internal or external surfaces in the body. Basal cell carcinomas develop in the skin, while adenocarcinomas can form in the glands.

When cancerous cells spread to other parts of the body, the medical term for this is metastasis.

A person can also have more than one type of cancer at a time.

Improvements in cancer detection, increased awareness of the risks of smoking, and a drop in tobacco use have all contributed to a year-on-year decrease in the number of cancer diagnoses and deaths.

According to the ACS, the overall cancer death rate declined by 33% between 1991 and 2020.

When a person has cancer, their outlook will depend on whether the disease has spread and on its type, severity, and location.

Frequently asked questions

Below are some common questions and answers about cancer.

How do I recognize cancer before it starts to cause serious health problems?

Some cancers cause early symptoms, but others do not exhibit symptoms until they are more advanced. Many of these symptoms are often from causes unrelated to cancer.

The best way to identify cancer early is to report any unusual, persistent symptoms to a doctor so they can offer advice about any further testing that may be needed.

Can people with cancer live a long life?

Each individual’s outlook varies depending on the type of cancer they have and other factors, such as their overall health and whether the disease has spread.

However, the ACS indicates that the overall cancer death rate has declined by 33% between 1991 and 2020.

How long can someone live with cancer without knowing?

Some types of cancer do not cause symptoms in the early stages. Therefore, a person may not know they are living with the disease until it reaches more advanced stages.

For example, research indicates that carcinoid tumors may not present with any symptoms for years .

Cancer causes cells to divide uncontrollably. It also prevents them from dying at the natural point in their life cycle.

Genetic factors and lifestyle choices, such as smoking, can contribute to the development of the disease. Several elements affect the ways that DNA communicates with cells and directs their division and death.

After nonmelanoma skin cancer, breast cancer is the most common type in the U.S.

Treatments are constantly improving. Examples of current methods include chemotherapy, radiation therapy, and surgery. Some people benefit from newer options, such as stem cell transplantation and precision medicine.

The diagnosis and death rates of cancer are dropping yearly.

Last medically reviewed on January 24, 2024

• Cancer / Oncology

How we reviewed this article:

• About cancer. (n.d.). https://www.cancer.gov/about-cancer
• All about cancer. (n.d.). https://www.cancer.org/cancer.html
• Cancer facts & figures 2023. (2023). https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2023/2023-cancer-facts-and-figures.pdf
• Cingam SR, et al. (2022). Carcinoid tumors. https://www.ncbi.nlm.nih.gov/books/NBK448101/
• Common cancer types. (2018). https://www.cancer.gov/types/common-cancers
• Risk factors and cancer. (2023). https://www.cdc.gov/cancer/risk_factors.htm

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Breast cancer.

Fadi M. Alkabban ; Troy Ferguson .

Affiliations

Last Update: September 26, 2022 .

• Continuing Education Activity

Breast cancer is the most common cancer diagnosed in women, accounting for more than 1 in 10 new cancer diagnoses each year. It is the second most common cause of death from cancer among women in the world. Breast cancer evolves silently, and most disease is discovered on routine screening. This activity reviews the pathophysiology, presentation and diagnosis of breast cancer and highlights the role of the interprofessional team in its management.

• Review the risk factors for breast cancer.
• Describe the histopathology of the different types of breast cancer.
• Summarize the treatment options for breast cancer.
• Outline modalities for improving care coordination among interprofessional team members to optimize outcomes for patients affected by breast cancer.
• Introduction

Breast cancer is the most common cancer diagnosed in women, accounting for more than 1 in 10 new cancer diagnoses each year. It is the second most common cause of death from cancer among women in the world. Anatomically, the breast has milk-producing glands in front of the chest wall. They lie on the pectoralis major muscle, and there are ligaments support the breast and attach it to the chest wall. Fifteen to 20 lobes circularly arranged to form the breast. The fat that covers the lobes determines the breast size and shape. Each lobe is formed by lobules containing the glands responsible for milk production in response to hormone stimulation. Breast cancer always evolves silently. Most of the patients discover their disease during their routine screening. Others may present with an accidentally discovered breast lump, change of breast shape or size, or nipple discharge. However, mastalgia is not uncommon. Physical examination, imaging, especially mammography, and tissue biopsy must be done to diagnose breast cancer. The survival rate improves with early diagnosis. The tumor tends to spread lymphatically and hematologically, leading to distant metastasis and poor prognosis. This explains and emphasizes the importance of breast cancer screening programs. [1] [2] [3]

Identifying factors associated with an increased incidence of breast cancer development is important in general health screening for women. [4] [5]  Risk factors for breast cancer can be divided into 7 broad categories:

• Age: The age-adjusted incidence of breast cancer continues to increase with the advancing age of the female population.
• Gender: Most breast cancers occur in women.
• Personal history of breast cancer: A history of cancer in one breast increases the likelihood of a second primary cancer in the contralateral breast.
• Histologic risk factors: Histologic abnormalities diagnosed by breast biopsy constitute an important category of breast cancer risk factors. These abnormalities include lobular carcinoma in situ (LCIS) and proliferative changes with atypia.
• The family history of breast cancer and genetic risk factors: First-degree relatives of patients with breast cancer have a 2-fold to 3-fold excess risk for developing the disease. Five percent to 10% of all breast cancer cases are due to genetic factors, but they may account for 25% of cases in women younger than 30 years. BRCA1 and BRCA2 are the 2 most important genes responsible for increased breast cancer susceptibility. 
• Reproductive risk factors: Reproductive milestones that increase a woman’s lifetime estrogen exposure are thought to increase her breast cancer risk. These include the onset of menarche before 12 years of age, first live childbirth after age 30 years, nulliparity, and menopause after age 55 years.
• Exogenous hormone use: Therapeutic or supplemental estrogen and progesterone are taken for various conditions, with the two most common scenarios being contraception in premenopausal women and hormone replacement therapy in postmenopausal women.
• Epidemiology

Invasive breast cancer affects 1 in 8 women in the United States (12.4%) during their lifetime. [6] [7] [8]  In the United States, about 266,120 women will have invasive breast carcinoma in 2018, and 63,960 will have in situ breast cancer. In 2018, approximately 2550 men will have invasive breast cancer. Approximately 1 in 1000 men will have breast cancer during their lifetime. In the year 2000, the incidence of breast cancer in the United States began decreasing. This decrease may be due to the reduced use of hormone replacement therapy (HRT) by women. A connection was suggested between HRT and increased breast cancer risk. About 40,920 US women may die in 2018 from breast cancer. Larger decreases occur in women younger than 50 years old. In 2008, there were an estimated 1.38 million new cases of invasive breast cancer worldwide. The 2008 incidence of female breast cancer ranged from 19.3 cases per 100,000 in Eastern Africa to 89.9 cases per 100,000 in Western Europe. With early detection and significant advances in treatment, death rates from breast cancer have been decreasing over the past 25 years in North America and parts of Europe. In many African and Asian countries (e.g., Uganda, South Korea, and India), however, breast cancer death rates are rising. The incidence rate of breast cancer increases with age, from 1.5 cases per 100,000 in women 20 to 24 years of age to a peak of 421.3 cases per 100,000 in women 75 to 79 years of age; 95% of new cases occur in women aged 40 years or older. The median age of women at the time of breast cancer diagnosis is 61 years. According to the American Cancer Society (ACS), breast cancer rates among women from various racial and ethnic groups are as follows:

• Non-Hispanic white: 128.1 in 100,000
• African American: 124.3 in 100,000
• Hispanic/Latina: 91.0 in 100,000
• American Indian/Alaska Native: 91.9 in 100,000
• Asian American/Pacific Islander: 88.3 in 100,000
• Pathophysiology

Breast cancer develops due to DNA damage and genetic mutations that can be influenced by exposure to estrogen. Sometimes there will be an inheritance of DNA defects or pro-cancerous genes like BRCA1 and BRCA2 . Thus the family history of ovarian or breast cancer increases the risk for breast cancer development. In a normal individual, the immune system attacks cells with abnormal DNA or abnormal growth. This fails in those with breast cancer disease leading to tumor growth and spread.

• Histopathology

Breast cancer can be invasive or non-invasive according to its relation to the basement membrane. Noninvasive neoplasms of the breast are broadly divided into two major types, lobular carcinoma in situ (LCIS) and ductal carcinoma in situ (DCIS).

LCIS is regarded as a risk factor for the development of breast cancer. LCIS is recognized by its conformity to the outline of the normal lobule, with expanded and filled acini. DCIS is more morphologically heterogeneous than LCIS, and pathologists recognize four broad types of DCIS: papillary, cribriform, solid, and comedo.

DCIS is recognized as discrete spaces filled with malignant cells, usually with a recognizable basal cell layer composed of presumably normal myoepithelial cells. The papillary and cribriform types of DCIS are generally lower grade lesions and may take longer to transform into invasive cancer.

The solid and comedo types of DCIS are generally higher-grade lesions. DCIS, if not treated, usually transforms into invasive cancer. Invasive breast cancers are recognized by their lack of overall architecture, infiltration of cells haphazardly into a variable amount of stroma, or formation of sheets of continuous and monotonous cells without respect for the form and function of a glandular organ. Pathologists broadly divide invasive breast cancer into ductal and lobular histologic types.

Invasive ductal cancer tends to grow as a cohesive mass; it appears as discrete abnormalities on mammograms and is often palpable as a discrete lump in the breast smaller than lobular cancers. Invasive lobular cancer tends to permeate the breast in a single-file nature, which explains why it remains clinically occult and often escapes detection on mammography or physical examination until the disease is extensive. Invasive ductal cancer, also known as infiltrating ductal carcinoma, is the most common form of breast cancer; it accounts for 50% to 70% of invasive breast cancers.

Invasive lobular carcinoma accounts for 10% of breast cancers, and mixed ductal and lobular cancers have been increasingly recognized and described in pathology reports. When invasive ductal carcinomas take on differentiated features, they are named according to the features that they display. If the infiltrating cells form small glands lined by a single row of the bland epithelium, they are called infiltrating tubular carcinoma. The infiltrating cells may secrete copious amounts of mucin and appear to float in this material. These lesions are called mucinous or colloid tumors.

Tubular and mucinous tumors are usually low-grade (grade I) lesions; these tumors account for approximately 2% to 3% of invasive breast carcinomas. Medullary cancer is characterized by bizarre invasive cells with high-grade nuclear features, many mitoses, and lack of an in situ component. The malignancy forms sheets of cells in an almost syncytial fashion, surrounded by an infiltrate of small mononuclear lymphocytes. The borders of the tumor push into the surrounding breast rather than infiltrate or permeate the stroma. In its pure form, medullary cancer accounts for only approximately 5% of breast cancers. [9] [10] [11]

• History and Physical

Most early breast cancer patients are asymptomatic and discovered during screening mammography. With increasing size, the patient may discover cancer as a lump that is felt accidentally, mostly during combing or showering. Breast pain is an unusual symptom that happens 5% of the time. The locally advanced disease may be presented with peau d'orange, frank ulceration, or fixation to the chest wall. Inflammatory breast cancer, an advanced form of breast cancer, frequently resembles breast abscess and presents with swelling, redness, and other local signs of inflammation. Paget disease of the nipple usually presents with nipple changes that must be differentiated from nipple eczema. 

Evaluation of Patients with breast cancer needs a triple assessment using clinical evaluation, imaging, and tissue biopsy. Mammography is the most commonly used modality for the diagnosis of breast cancer. Most of the asymptomatic cases are diagnosed during screening mammography. Breast cancer always presents as calcifications, dense lump, with or without architecture distortion. However, mammography is not sensitive in young women for whom breast ultrasonography can be used. Ultrasonography is useful in assessing the consistency and size of breast lumps. It has a great role in guided needle biopsy. Magnetic resonance imaging has good sensitivity for describing abnormalities in soft tissues, including the breast. It is indicated if there are occult lesions, or suspicion of multifocal or bilateral malignancy, especially ILC, and in the assessment of response to neoadjuvant chemotherapy, or when planning for breast conservation surgery and screening in the high-risk patient. Tissue biopsy is an important step in the evaluation of a breast cancer patient. There are different ways to take a tissue specimen, and these include fine-needle aspiration cytology, core biopsy (Trucut), and incisional or excisional biopsy. [12] [13] [14]

• Treatment / Management

The 2 basic principles of treatment are to reduce the chance of local recurrence and the risk of metastatic spread. Surgery with or without radiotherapy achieves local control of cancer. When there is a risk for metastatic relapse, systemic therapy is indicated in the form of hormonal therapy, chemotherapy, targeted therapy, or any combination of these. In locally advanced disease, systemic therapy is used as a palliative therapy with a small or no role for surgery. [15] [16] [17]

• Differential Diagnosis
• Breast abscess
• Fat necrosis
• Fibroadenoma
• Surgical Oncology

Surgery has a major role in the treatment of breast cancer. It is the basic way to use for local control of the disease. Radical mastectomy of Halsted, which removed the breast with axillary lymph node dissection and excision of both pectoralis muscles, is no longer recommended due to the high rate of morbidity without a survival benefit. Now, the modified radical mastectomy of Patey is more famous. It entails removing the whole breast tissue with a large part of the skin and the axillary lymph nodes. The pectoralis major and minor muscles are preserved. Breast-only removal without axillary dissection is referred to as simple mastectomy. This procedure can be performed in small tumors with negative sentinel lymph nodes. Breast-conserving surgery (BCS) is aimed at removing the tumor plus a rim of at least 1 cm of normal breast tissue (wide local excision). A quadrantectomy involves removing the entire segment of the breast that contains the tumor. The last 2 procedures are usually combined with axillary clearance through a separate incision. Axillary procedures may include sentinel lymph node biopsy, sampling, partial (II), or complete (III) axillary lymph node dissection. Lumpectomy is the removal of a benign mass without excision of the normal breast tissue.

• Radiation Oncology

Radiation therapy has a significant role in local disease control. The risk of cancer recurrence decreases by about 50% at 10 years, and the risk of breast cancer death reduces by almost 20% at 15 years when radiation therapy follows BCS. However, radiation is not necessary for women 70 years of age and older with small, lymph node-negative, hormone receptor-positive (HR+) cancers because it has not been shown to improve survival in patients who take hormonal therapy for at least 5 years. Radiation therapy is beneficial in large tumors (greater to 5 cm) or if the tumor invades skin or chest wall and if there are positive lymph nodes. It can also be used as palliative therapy in advanced cases, such as a central nervous system (CNS) or bone metastasis. It can be delivered as external beam radiation, brachytherapy, or a combination of both. [18] [19]

• Medical Oncology

Chemotherapy, hormone therapy, and targeted therapy are the systemic therapies used in breast cancer management. A 25 percent reduction in the risk of relapse over a 10 to 15-year period using a first-generation chemotherapy regimen such as cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) in a 6-month cycle. Anthracyclines (doxorubicin or epirubicin) and the newer agents such as the taxanes are modern regimens used for breast cancer. Three to 6-month period is used for adjuvant and neoadjuvant chemotherapy. Adjuvant treatment of early-stage HR+ breast cancer with tamoxifen for at least 5 years has been shown to reduce the recurrence rate by about half throughout the first 10 years and reduces breast cancer mortality by about 30% throughout the first 15 years.

More recently, studies have shown that extended use of adjuvant tamoxifen (10 years versus 5 years) further reduces the risk of breast cancer recurrence and mortality, so clinical practice guidelines now recommend consideration of adjuvant tamoxifen therapy for 10 years. The mainstay of treatment for most premenopausal women with HR+ tumors is tamoxifen. Some women may also benefit from surgical removal (oophorectomy) or chemical suppression of the ovaries, which are the main source of estrogen before menopause. Treatment guidelines recommend aromatase inhibitors (AIs) such as anastrozole should usually be included in the treatment of postmenopausal women with HR+ breast cancer. Targeted therapy is usually indicated in about 17% of breast cancers that overproduce the growth-promoting protein HER2/neu. Trastuzumab, the first approved drug, is a monoclonal antibody that directly targets the HER2 protein. It reduces the risk of recurrence and death by 52% and 33%, respectively, if combined with chemotherapy in HER2+ early breast cancer if compared to chemotherapy alone. [20] [21]

Breast cancer staging is determined clinically by physical examination and imaging studies before treatment, and breast cancer stage is determined pathologically by pathologic examination of the primary tumor and regional lymph nodes after definitive surgical treatment. Staging is performed to group patients into risk categories that define prognosis and guide treatment recommendations for patients with a similar prognosis. Breast cancer is classified with the TNM classification system, which groups patients into 4 stage groupings based on the primary tumor size (T),  the regional lymph nodes status (N), and if there is any distant metastasis (M). The most widely used system is that of the American Joint Committee on Cancer:

Primary Tumor (T)  

Tis: Carcinoma in-situ, Paget‘s with no tumor

T1: Less than 2 cmT1a: 0.1 to 0.5 cmT1b: 0.5 to 1.0 cmT1c: 1.0 to 2.0 cm

T2: 2 to 5 cm

T3: Larger than 5 cm

T4 T4a: Chest wall involvementT4b: Skin involvementT4c: Both 4a and 4bT4d: Inflammatory ca

Regional Lymph Nodes (N)

N1: Mobile ipsilateral axillary nodes

N2: Fixed/matted ipsilateral axillary nodes

N3 N3a – Ipsilat infraclavicular nodesN3b – Ipsilat int mammary nodesN3c – Ipsilateral supraclavicular nodes

Distant Metastases (M)

M1: Distant metastases

Stage 0     Tis

Stage I T1N0

Stage II T2N0, T3N0 T0N1, T1N1, T2N1

Stage III 

*skin, rib inv., matted LNs T3 N1 T0N2, T1N2, T2N2, T3N2 Any T, N3 T4, any N Locally advanced BC

The prognosis of early breast cancer is quietly good. Stage 0 and stage I both have a 100% 5-year survival rate. The 5-year survival rate of stage II and stage III breast cancer is about 93% and 72%, respectively. When the disease spreads systemically, its prognosis worsens dramatically. Only 22% of stage IV breast cancer patients will survive their next 5 years.

• Complications

Complications can arise from the treatment, whether chemotherapy, radiation, hormonal therapy, or surgery.

Surgical complications include:

• Cosmetic issues
• Permanent scarring
• Alteration or loss of sensation in the chest area and reconstructed breasts

Chemotherapy complications include:

• Nausea/vomiting and diarrhea
• Memory loss ("chemo brain")
• Vaginal dryness
• Menopausal symptoms/fertility issues

Complications accompanying hormonal therapy include:

• Hot flashes
• Vaginal discharge dryness
• Impotence in males with breast cancer

Radiation can result in the following complications:

• Pain and skin changes
• Heart and lung issues (long-term)
• Deterrence and Patient Education

Patients usually require counseling to deal with the condition and treatment. They should be put in touch with psychological counseling, and there are also support groups available.

• Pearls and Other Issues

Breast cancer patients are advised to be followed up for life to detect early recurrence and spread. Yearly or biannual follow-up mammography is recommended for the treated and the other breast. The patient must be informed that they must visit a breast clinic if they have any suspicious manifestations. Currently, there is no role for repeated measurements of tumor markers or doing follow-up imaging other than mammography.

• Enhancing Healthcare Team Outcomes

After the treatment of breast cancer, long-term follow-up is necessary. There is a risk of local and distant relapse, and hence an interprofessional team approach is necessary. The women need regular mammograms and a pelvic exam. Also, women with risk factors for osteoporosis need a bone density exam and monitoring for tumor markers for metastatic disease. For those who are about to undergo radiation therapy, a baseline echo and cardiac evaluation are necessary. Even though many types of integrative therapies have been developed to help women with breast cancer, evidence for the majority of these treatments is weak or lacking. [22]

Over the past four decades, the survival rates of most breast cancer patients have improved. Of note is that the presence of breast cancer has gradually slowed down over the past decade, which may be due to earlier detection and improved treatments. The prognosis for patients with breast cancer is highly dependent on the status of axillary lymph nodes. The higher the number of positive lymph nodes, the worse the outcome. In general, hormone-responsive tumors tend to have a better outcome. In breast cancer survivors, adverse cardiac events are common; this is partly due to the cardiotoxic drugs to treat cancer and the presence of traditional risk factors for heart disease. The onus is on the healthcare provider to reduce the modifiable risk factors and lower the risk of adverse cardiac events. [1] [23]  [Level 5)

• Review Questions
• Access free multiple choice questions on this topic.
• Comment on this article.

Breast Cancer Metastasis Sites Medical Gallery of Mikael Häggström 2014, Public Domain, via Wikimedia Commons. 

Breast Mammogram. A mammographic view of the left breast demonstrates skin thickening, diffusely increased breast density, and malignant type calcifications in this patient with biopsy-proven inflammatory breast cancer. Contributed by Hassana (more...)

Breast Cancer Risk Factors 5. Kerlikowske K, Gard CC, Tice JA, et al. for the Breast Cancer Surveillance Consortium. Risk factors that increase risk of estrogen receptor-positive and -negative breast cancer. J Natl Cancer Inst. 109(5): djw276, 2016.

Interprofessional care diagram Breast cancer patients Contributed by Kathryn Malherbe (PhD candidate)

Breast Estrogen Receptor Staining Contributed by Fabiola Farci, MD

Breast Cancer Axillary Lymphadenopathy Contributed by Sunil Munakomi, MD

Breast Cancer Fine Needle Aspiration Cytology Contributed by Sunil Munakomi, MD

Clinical Signs of Breast Carcinoma Contributed by Sunil Munakomi, MD

Disclosure: Fadi Alkabban declares no relevant financial relationships with ineligible companies.

Disclosure: Troy Ferguson declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Alkabban FM, Ferguson T. Breast Cancer. [Updated 2022 Sep 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Antigen presentation in cancer — mechanisms and clinical implications for immunotherapy

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Nature Reviews Clinical Oncology volume  20 ,  pages 604–623 ( 2023 ) Cite this article

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• Immunotherapy
• Predictive markers
• Tumour immunology

Over the past decade, the emergence of effective immunotherapies has revolutionized the clinical management of many types of cancers. However, long-term durable tumour control is only achieved in a fraction of patients who receive these therapies. Understanding the mechanisms underlying clinical response and resistance to treatment is therefore essential to expanding the level of clinical benefit obtained from immunotherapies. In this Review, we describe the molecular mechanisms of antigen processing and presentation in tumours and their clinical consequences. We examine how various aspects of the antigen-presentation machinery (APM) shape tumour immunity. In particular, we discuss genomic variants in HLA alleles and other APM components, highlighting their influence on the immunopeptidomes of both malignant cells and immune cells. Understanding the APM, how it is regulated and how it changes in tumour cells is crucial for determining which patients will respond to immunotherapy and why some patients develop resistance. We focus on recently discovered molecular and genomic alterations that drive the clinical outcomes of patients receiving immune-checkpoint inhibitors. An improved understanding of how these variables mediate tumour–immune interactions is expected to guide the more precise administration of immunotherapies and reveal potentially promising directions for the development of new immunotherapeutic approaches.

The clinical success of immune-checkpoint inhibitors has improved cancer care, although long-term durable remission is only achieved in a subset of patients.

Antigen processing and presentation by tumour cells are essential for long-lasting immune surveillance.

Alterations in the genes encoding MHC components and other parts of the antigen-presentation machinery are frequently found across several cancer types and are associated with both tumour development and the effectiveness of immunotherapies.

MHC-based antigen presentation exerts strong evolutionary pressure on the immunopeptidome, which in turn shapes the mutational landscape of the tumour genome.

Germline human leukocyte antigen diversity and somatic aberrations in the antigen-presentation machinery inform the therapeutic response to immune-checkpoint inhibitors.

Development of novel therapies based on an accurate understanding of antigen presentation in the setting of tumour–immune dynamics is crucial to the development of improved therapeutic approaches.

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Acknowledgements

The authors are grateful for the support from NIH grants R35CA232097 (T.A.C.), R01CA205426 (T.A.C.), U54CA274513 (T.A.C.) and T32CA094186 (K.Y.), a Young Investigator Award from ASCO Conquer Cancer Foundation (K.Y.), a RSNA Research Resident Grant (K.Y.), and a Cleveland Clinic VeloSano Impact Award (K.Y.).

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Kailin Yang, Ahmed Halima & Timothy A. Chan

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T.A.C. is a co-founder of and holds equity in Gritstone Oncology; holds equity in An2H; acknowledges grant funding from An2H, AstraZeneca, Bristol Myers Squibb, Eisai, Illumina and Pfizer; has served as an advisor for An2H, AstraZeneca, Bristol Myers Squibb, Eisai, Illumina and MedImmune; and holds ownership of intellectual property on using tumour mutational burden to predict immunotherapy response, which has been licensed to PGDx. K.Y. and A.H. declare no competing interests.

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Yang, K., Halima, A. & Chan, T.A. Antigen presentation in cancer — mechanisms and clinical implications for immunotherapy. Nat Rev Clin Oncol 20 , 604–623 (2023). https://doi.org/10.1038/s41571-023-00789-4

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• 10. Cancer can occur at any age, but 67% of cancer deaths occur in people older than 65 years
• 11. CANCER STATISTICS 30% 25% 20% 15% 10% death % 5% 0% Heart Cancer chronic Diabetes Alzheimer disease respiratory disease lower diseases
• 12. There are two types of tumours: Malignant tumors spread to other areas in the body. Benign tumors stay in one place.
• 13. Main Features
• 14. Common environmental factors leading to cancer death include: tobacco (25-30%)
• 15. Common environmental factors leading to cancer death include: diet and obesity (30-35%) tobacco (25-30%)
• 16. Common environmental factors leading to cancer death include: diet and obesity (30-35%) tobacco (25-30%) infections (15-20%)
• 17. Common environmental factors leading to cancer death include: diet and obesity (30-35%) tobacco (25-30%) Radiation infections (15-20%) Stress lack of physical activity environmental pollutants
• 18. CAUSES Benzene and other chemicals Drinking excess alcohol Environmental toxins, such as certain poisonous mushrooms and a type of poison that can grow on peanut plants (aflatoxins) Excessive sunlight exposure Genetic problems Obesity Radiation Viruses
• 20. Bladder Cancer
• 21. Bladder Cancer Lung Cancer
• 22. Bladder Cancer Lung Cancer Breast Cancer
• 23. Bladder Cancer Lung Cancer Breast Cancer Melanoma
• 24. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer
• 25. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma
• 26. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma Endometrial Cancer
• 27. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma Endometrial Cancer Pancreatic Cancer
• 28. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma Endometrial Cancer Pancreatic Cancer Kidney (Renal Cell) Cancer
• 29. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma Endometrial Cancer Pancreatic Cancer Kidney (Renal Cell) Cancer Prostate Cancer
• 30. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma Endometrial Cancer Pancreatic Cancer Kidney (Renal Cell) Cancer Prostate Cancer Thyroid Cancer
• 31. Bladder Cancer Lung Cancer Breast Cancer Melanoma Colon and Rectal Cancer Non-Hodgkin Lymphoma Endometrial Cancer Pancreatic Cancer Kidney (Renal Cell) Cancer Prostate Cancer Thyroid Cancer
• 32. Leukemia
• 33. TESTS Biopsy of the tumor Blood tests (which look for chemicals such as tumor markers) Bone marrow biopsy (for lymphoma or leukemia) Chest x-ray Complete blood count (CBC) CT scan Liver function tests MRI scan
• 34. TREATMENT & PREVENTION
• 35. TREATMENT •Surgery •Chemotherapy •Radiation •Targeted Cancer Treatments •Small Molecule Inhibitors •Antibodies •Cell Based Immunotherapy •Gene Therapy
• 36. Chemotherapy Drugs used to kill cancer cells; disrupt some aspect of cell division. Toxic to healthy cells; hair, bone marrow, lymphocytes, and epithelial cells of intestinal lining . Side effects include hair loss, nausea, vomiting, and reduced immune responses.
• 37. Radiation therapy High-energy rays are used to kill cancer cells  Stop them from growing and dividing. radiotherapy is a local treatment; it can affect cancer cells only in the treated area. side effects- Tiredness, skin reactions such as rash or redness, and loss of appetite. Temporary lowering of the WBC count.
• 38. Surgery therapy In localized cancer surgery typically attempts to remove the entire mass. Biological therapy/immunotherapy  Monoclonal antibodies, interferon, interleukin- 2, and colony-stimulating factors. Side effects - Temporary flu-like symptoms such as fever and chills, muscle aches and weakness, loss of appetite and diarrhea.
• 39. Recently launched drugs- Axitinib (Inlyta) for advanced kidney cancer. Vismodegib (Erivedge) for advanced basal cell carcinoma. Carfilzomib (Kyprolis) for multiple myeloma. Ziv-aflibercept (Zaltrap) in combination with chemotherapy for metastatic colon cancer. Regorafenib (Stivarga) for metastatic colorectal cancer .
• 40. PREVENTION Eating a healthy diet. Exercising regularly. Limiting alcohol. Maintaining a healthy weight. Minimizing your exposure to radiation and toxic chemicals. Not smoking or chewing tobacco Reducing sun exposure, especially if you burn easily.
• 41. CONCLUSION Hence cancer is second leading cause of deaths following heart diseases one should care about its prevention before the occurrence of disease by varies examinations and if disease is already exists then one should go for its regular treatment. Recent treatment mainly includes radiation therapy, cell based immunotherapy, gene therapy, chemotherapy are most widely used methods used for treatment of various type of cancers.
• 42. REFERNCES www.chronicdisease.isdh.in www.cancer.gov www.chronicdisease.isdh.in.gov http://www.essense-of-life.com/moreinfo/minerals/cesium.htm http://www.micronmetals.com/55.htm http://www.stopcancer.com/toc.htm http://www.prostate90.com/sci_papers/warburg.html http://www.alternative-doctor.com/cancer/oxygen.htm http://www.advancedhealthplan.com/2cesiumchlorideforcancer2.html Cancer Facts and Figures 2012". Journalist's Resource.org http://www.medicalnewstoday.com/info/cancer-oncology http://www.news-medical.net/health/What-is-Cancer.aspx http://www.cancerresearchuk.org/ http://www.who.int/cancer/

Colorectal cancer cases more than tripled among teens over two decades, data show

C olorectal cancer incidence has steadily increased among younger people in the U.S. over the last two decades, with the youngest seeing the most dramatic jumps, according to a study scheduled for presentation at Digestive Disease Week (DDW) 2024. Between 1999 and 2020, the rate of colorectal cancers grew 500% among children ages 10 to 14, 333% among teens aged 15 to 19, and 185% among young adults ages 20 to 24, researchers said.

"Colorectal cancer is no longer considered just a disease of the elderly population," said lead researcher Islam Mohamed, MD, an internal medicine resident physician at the University of Missouri-Kansas City. "It's important that the public is aware of signs and symptoms of colorectal cancer."

Risk factors include a family history of inflammatory bowel disease or colorectal cancer. Modifiable risk factors include obesity, tobacco use, alcohol consumption and dietary habits such as low fiber intake, consumption of processed meats or sugar-sweetened beverages and a high-fat diet. Sedentary lifestyle, the presence of bacteria that tend to cause tumors, antibiotic usage, and dietary additives are potential, but not firmly established, contributors to colorectal cancer risk.

Using data from the Centers for Disease Control Wonder Database, Mohamed's team calculated trends in colorectal cancer rates for people ages 10 to 44 from 1999 to 2020.

The number of colorectal cancer cases among children and teens is not high enough to suggest widespread colonoscopy screening, but more tailored approaches should be considered, Mohamed said. In 2020, only .6 children ages 10 to14 per 100,000 population were diagnosed compared to .1 per 100,000 in 1999. Diagnoses in teens age 15 to 19 went from .3 to 1.3 per 100,000, and in young adults ages 20 to 24, cases rose from .7 to 2 per 100,000.

The most common symptoms for colorectal cancer identified in patients with early onset colorectal cancer were changes in bowel habits in terms of either constipation or diarrhea, abdominal pain, rectal bleeding and signs of iron deficiency anemia, Mohamed said.

Escalations were also found in the higher age brackets, with rates rising by 71% to 6.5 per 100,000 people in ages 30 to 34 and by 58% to 11.7 per 100,000 in ages 35 to 39 in 2020. While the 40-to-44 age group had a lower percentage increase of 37%, this group had the highest incidence rate, reaching 20 per 100,000 people in 2020.

Dr. Mohamed will present data from the study, "Evolving trends in colorectal cancer incidence among young patients under 45: A 22-year analysis of the Centers for Disease Control Wonder Database," abstract Mo1149, on Monday, May 20, at 12:30 p.m. EDT.

Provided by Digestive Disease Week

Lecia V. Sequist, MD, MPH - Screening and Early Intervention as the Keys to Success in Lung Cancer: A Practical Approach to Implementing Lung Cancer Screening for High-Risk Individuals PeerView Oncology & Hematology CME/CNE/CPE Audio Podcast

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups. For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/PJP865. CME/MOC/AAPA/IPCE credit will be available until April 16, 2025. Screening and Early Intervention as the Keys to Success in Lung Cancer: A Practical Approach to Implementing Lung Cancer Screening for High-Risk Individuals In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and LUNGevity Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team. Support This activity is supported by an educational grant from Merck & Co., Inc. Disclosure information is available at the beginning of the video presentation.

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Clinical Benefit From Immunotherapy in Patients With SCLC Is Associated With Tumor Capacity for Antigen Presentation

Affiliations.

• 1 Thoracic Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York; Department of Medicine, Weill Cornell Medical College, New York, New York; Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York. Electronic address: [email protected].
• 2 Bristol-Myers Squibb, New York, New York.
• 3 Thoracic Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York; Department of Medicine, Weill Cornell Medical College, New York, New York.
• 4 Marie-Josée and Henry R. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York.
• 5 Cancer Biology Program, Louis V. Gerstner Jr. Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, New York.
• 6 Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
• 7 Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
• 8 Perlmutter Cancer Center, New York University Langone Health, New York, New York.
• PMID: 37210008
• PMCID: PMC10524620 (available on 2024-09-01 )
• DOI: 10.1016/j.jtho.2023.05.008

Introduction: A small percentage of patients with SCLC experience durable responses to immune checkpoint blockade (ICB). Defining determinants of immune response may nominate strategies to broaden the efficacy of immunotherapy in patients with SCLC. Prior studies have been limited by small numbers or concomitant chemotherapy administration.

Methods: CheckMate 032, a multicenter, open-label, phase 1/2 trial evaluating nivolumab alone or with ipilimumab was the largest study of ICB alone in patients with SCLC. We performed comprehensive RNA sequencing of 286 pretreatment SCLC tumor samples, assessing outcome on the basis of defined SCLC subtypes (SCLC-A, -N, -P, and -Y), and expression signatures associated with durable benefit, defined as progression-free survival more than or equal to 6 months. Potential biomarkers were further explored by immunohistochemistry.

Results: None of the subtypes were associated with survival. Antigen presentation machinery signature (p = 0.000032) and presence of more than or equal to 1% infiltrating CD8+ T cells by immunohistochemistry (hazard ratio = 0.51, 95% confidence interval: 0.27-0.95) both correlated with survival in patients treated with nivolumab. Pathway enrichment analysis revealed the association between durable benefit from immunotherapy and antigen processing and presentation. Analysis of epigenetic determinants of antigen presentation identified LSD1 gene expression as a correlate of worse survival outcomes for patients treated with either nivolumab or the combination of nivolumab and ipilimumab.

Conclusions: Tumor antigen processing and presentation is a key correlate of ICB efficacy in patients with SCLC. As antigen presentation machinery is frequently epigenetically suppressed in SCLC, this study defines a targetable mechanism by which we might improve clinical benefit of ICB for patients with SCLC.

Keywords: Antigen presentation; Epigenetics; Immune checkpoint blockade; Small cell lung cancer.

Copyright © 2023 International Association for the Study of Lung Cancer. Published by Elsevier Inc. All rights reserved.

Publication types

• Clinical Trial, Phase II
• Clinical Trial, Phase I
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• Nivolumab / therapeutic use
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Oncoexporter: Conversion of NCI CRDC Data to the GA4GH Phenopacket Schema

If you’re attending the EACR 2024, make sure you hear Dr. Daoud Meerzaman’s poster presentation on using Oncoexporter to convert Cancer Research Data Commons (CRDC) data into the Global Alliance for Genomics and Health (GA4GH) Phenopackets schema. 

Dr. Meerzaman will illustrate the application of the Phenopacket standard to CRDC data and demonstrate a subsequent application to a simple clinical analysis.

Providing tools to convert CRDC data into the Phenopacket schema will enable further integration and analysis of a broad array of cancer data. This integration could unlock important insights into cancer development, progression, and treatment hidden in the massive reservoirs of heterogeneous cancer data sets worldwide.

The GA4GH Phenopacket schema is a common framework for capturing phenotypic and genotypic data in a way that works well with downstream machine learning applications. 

The CRDC is a cloud-based infrastructure that provides public and controlled access to multiple large-scale cancer data sets . You can use NCI Cloud Resources to analyze these data sets without downloading.

Dr. Meerzaman is the Computational Genomics and Bioinformatics Branch chief at NCI’s Center for Biomedical Informatics and Information Technology. Dr. Meerzaman and his team provide bioinformatics analysis support for life sciences and clinical and translational research for intramural scientists, including NCI’s Division of Cancer Epidemiology and Genetics and Center for Cancer Research.

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Arvinas announces upcoming vepdegestrant poster presentations at the 2024 european society for medical oncology (esmo) breast cancer annual congress.

NEW HAVEN, Conn., May 09, 2024 (GLOBE NEWSWIRE) -- Arvinas, Inc. (Nasdaq: ARVN) today announced that two posters, including updated clinical trial data, for vepdegestrant will be presented at the 2024 European Society for Medical Oncology (ESMO) Breast Cancer Annual Congress held from May 15-17, 2024, in Berlin, Germany. Vepdegestrant is a novel investigational PROTAC ® estrogen receptor (ER) degrader that is being jointly developed by Arvinas and Pfizer for the treatment of patients with early and locally advanced or metastatic ER positive/human epidermal growth factor receptor 2 (HER2) negative (ER+/HER2-) breast cancer.

Poster session details are as follows: Date: Thursday, May 16, 2024 Time: 12:00 – 1:00 p.m. CET/ 6:00 – 7:00 a.m. ET Category: Metastatic Breast Cancer

Poster Title and Number: Vepdegestrant, a PROteolysis TArgeting Chimera (PROTAC) estrogen receptor (ER) degrader, plus palbociclib (palbo) in ER+/human epidermal growth factor receptor 2 (HER2)- advanced breast cancer: updated phase 1b cohort results, Poster 218P Presentation Type and Abstract Number: Abstract, 453

Poster Title and Number: TACTIVE-K: phase 1b/2 study of vepdegestrant, a PROteolysis TArgeting Chimera (PROTAC) estrogen receptor (ER) degrader, in combination with PF-07220060, a cyclin-dependent kinase (CDK)4 inhibitor, in ER+/human epidermal growth factor receptor 2 (HER2)- advanced breast cancer, Poster 264 Presentation Type and Abstract Number: Trial-in-Progress (TiP), 488

Abstracts are now available via the official ESMO Breast Cancer Annual Congress website here .

About Vepdegestrant Vepdegestrant is an investigational, orally bioavailable PROTAC protein degrader designed to specifically target and degrade the estrogen receptor (ER) for the treatment of patients with ER positive (ER+)/human epidermal growth factor receptor 2 (HER2) negative (ER+/HER2-) breast cancer. Vepdegestrant is being developed as a potential monotherapy and as part of combination therapy across multiple treatment settings for ER+/HER2- metastatic breast cancer.

In July 2021, Arvinas announced a global collaboration with Pfizer for the co-development and co-commercialization of vepdegestrant; Arvinas and Pfizer will share worldwide development costs, commercialization expenses, and profits.

The U.S. Food and Drug Administration (FDA) has granted vepdegestrant Fast Track designation as a monotherapy in the treatment of adults with ER+/HER2- locally advanced or metastatic breast cancer previously treated with endocrine-based therapy.

About Arvinas Arvinas is a clinical-stage biotechnology company dedicated to improving the lives of patients suffering from debilitating and life-threatening diseases through the discovery, development, and commercialization of therapies that degrade disease-causing proteins. Arvinas uses its proprietary PROTAC ® Discovery Engine platform to engineer proteolysis targeting chimeras, or PROTAC ® targeted protein degraders, that are designed to harness the body’s own natural protein disposal system to selectively and efficiently degrade and remove disease-causing proteins. In addition to its robust preclinical pipeline of PROTAC protein degraders against validated and “undruggable” targets, the company has four investigational clinical-stage programs: vepdegestrant for the treatment of patients with locally advanced or metastatic ER+/HER2- breast cancer; ARV-766 and bavdegalutamide for the treatment of men with metastatic castration-resistant prostate cancer; and ARV-102 for the treatment of patients with neurodegenerative disorders. For more information, visit www.arvinas.com .

Forward-Looking Statements This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties, including statements regarding plans with respect to vepdegestrant as a potential monotherapy and combination across multiple treatment settings for ER+/HER2- metastatic breast cancer. All statements, other than statements of historical facts, contained in this press release, including statements regarding Arvinas’ strategy, future operations, future financial position, future revenues, projected costs, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “estimate,” “expect,” “intend,” “may,” “might,” “plan,” “predict,” “project,” “target,” “potential,” “will,” “would,” “could,” “should,” “continue,” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words.

Arvinas may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on such forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements Arvinas makes as a result of various risks and uncertainties, including but not limited to: Arvinas’ and Pfizer, Inc.’s (“Pfizer”) performance of the respective obligations with respect to Arvinas’ collaboration with Pfizer; whether Arvinas and Pfizer will be able to successfully conduct and complete clinical development for vepdegestrant (ARV-471); whether Arvinas and Pfizer, as appropriate, will be able to obtain marketing approval for and commercialize vepdegestrant (ARV-471)on current timelines or at all; Arvinas’ ability to protect its intellectual property portfolio; whether Arvinas’ cash and cash equivalent resources will be sufficient to fund its foreseeable and unforeseeable operating expenses and capital expenditure requirements; and other important factors discussed in the “Risk Factors” section of Arvinas’ Annual Report on Form 10-K for the year ended December 31, 2023 and subsequent other reports on file with the U.S. Securities and Exchange Commission. The forward-looking statements contained in this press release reflect Arvinas’ current views with respect to future events, and Arvinas assumes no obligation to update any forward-looking statements, except as required by applicable law. These forward-looking statements should not be relied upon as representing Arvinas’ views as of any date subsequent to the date of this release.

Investors: Jeff Boyle +1 (347) 247-5089 [email protected]

Media: Kathleen Murphy +1 (760) 622-3771 [email protected]

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Abivax announces presentation of four abstracts for obefazimod in ulcerative colitis and preclinical colon cancer model at Digestive Disease Week 2024

PARIS, France, May 8, 2024, 8:30 a.m. CEST – Abivax SA (Euronext Paris & Nasdaq: ABVX) (“Abivax” or the “Company”), a clinical-stage biotechnology company focused on developing therapeutics that harness the body’s natural regulatory mechanisms to stabilize the immune response in patients with chronic inflammatory diseases, today announced that four scientific abstracts on its lead drug candidate, obefazimod, for the treatment of moderately to severely active ulcerative colitis (UC) and in a preclinical model on colon cancer, will be presented at Digestive Disease Week (DDW) as part of scientific exchange, taking place May 18-21, 2024, in Washington D.C., U.S.

“With four abstracts accepted for presentation at DDW 2024, we look forward to our continued exchange with the IBD community around the emerging clinical profile of obefazimod,” said Sheldon Sloan, M.D., M. Bioethics, Chief Medical Officer of Abivax. “We are excited to share new preclinical data showing obefazimod’s impact in reducing the number of tumors in the azoxymethane (AOM)/dextran sodium sulfate (DSS) mouse model of colitis-associated cancer—data in support of obefazimod’s novel mechanism of action.”

For more information, visit the Abivax booth at the DDW exhibitor hall (booth #529) or see congress details on the DDW website . Obefazimod data to be presented:

Abivax has also sponsored a Product Theater presentation titled, “ An Investigational New MOA that Can Stabilize the Inflammatory Response in Ulcerative Colitis ,” taking place on May 20, 2024, at 2:30-3:15 p.m. EDT in room “DDW Theater 1,” featuring Prof. Parambir S. Dulai, M.D., Associate Professor of Medicine in the Division of Gastroenterology and Hepatology at Northwestern University, Evanston, Illinois, U.S.

About Obefazimod Obefazimod, Abivax’s lead investigational drug candidate, is an orally administered small molecule that was demonstrated to potentially enhance the expression of a single microRNA, miR-124. Phase 2 clinical trials in patients with UC have generated positive data, resulting in the initiation of a pivotal global Phase 3 clinical trial program (ABTECT Program), with first patients enrolled in the United States in October 2022. Initiation of a Phase 2b clinical trial in Crohn’s disease is expected in Q3 2024, and exploration of potential combination therapy opportunities in UC is ongoing.

About Abivax Abivax is a clinical-stage biotechnology company focused on developing therapeutics that harness the body’s natural regulatory mechanisms to stabilize the immune response in patients with chronic inflammatory diseases. Based in France and the United States, Abivax’s lead drug candidate, obefazimod (ABX464), is in Phase 3 clinical trials for the treatment of moderately to severely active ulcerative colitis. More information on the Company is available at www.abivax.com . Follow us on LinkedIn and on X, formerly Twitter, @Abivax. Contact:

Abivax Investor Relations Patrick Malloy [email protected] +1 847 987 4878

Abivax Communications [email protected]

FORWARD-LOOKING STATEMENTS

This press release contains forward-looking statements, forecasts and estimates, including those relating to the Company’s business and financial objectives. Words such as “design,” “expect,” “forward,” “future,” “potential,” “plan,” “project” and variations of such words and similar expressions are intended to identify forward-looking statements. Although Abivax’s management believes that the expectations reflected in such forward-looking statements are reasonable, investors are cautioned that forward-looking information and statements are subject to various risks, contingencies and uncertainties, many of which are difficult to predict and generally beyond the control of Abivax, that could cause actual results and developments to differ materially from those expressed in, or implied or projected by, the forward-looking information and statements. A description of these risks, contingencies and uncertainties can be found in the documents filed by the Company with the French Autorité des Marchés Financiers pursuant to its legal obligations including its universal registration document (Document d’Enregistrement Universel) and in our Annual Report on Form 20-F filed with the U.S. Securities and Exchange Commission on April 5, 2024 under the caption “Risk Factors.” These risks, contingencies and uncertainties include, among other things, the uncertainties inherent in research and development, future clinical data and analysis, decisions by regulatory authorities, such as the FDA or the EMA, regarding whether and when to approve any drug candidate, as well as their decisions regarding labelling and other matters that could affect the availability or commercial potential of such product candidates. Special consideration should be given to the potential hurdles of clinical and pharmaceutical development including further assessment by the company and regulatory agencies and IRBs/ethics committees following the assessment of preclinical, pharmacokinetic, carcinogenicity, toxicity, CMC and clinical data. Furthermore, these forward-looking statements, forecasts and estimates are only as of the date of this press release. Readers are cautioned not to place undue reliance on these forward-looking statements. Abivax disclaims any obligation to update these forward-looking statements, forecasts or estimates to reflect any subsequent changes that the Company becomes aware of, except as required by law. Information about pharmaceutical products (including products currently in development) that is included in this press release is not intended to constitute an advertisement. This press release is for information purposes only, and the information contained herein does not constitute either an offer to sell, or the solicitation of an offer to purchase or subscribe securities of the Company in any jurisdiction. Similarly, it does not give and should not be treated as giving investment advice. It has no connection with the investment objectives, financial situation or specific needs of any recipient. It should not be regarded by recipients as a substitute for exercise of their own judgment. All opinions expressed herein are subject to change without notice. The distribution of this document may be restricted by law in certain jurisdictions. Persons into whose possession this document comes are required to inform themselves about and to observe any such restrictions.

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