essay on cancer cells

What Is Cancer?

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Breast cancer cell dividing, as seen using microscope.

A dividing breast cancer cell.

The Definition of Cancer

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

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

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

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

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

Differences between Cancer Cells and Normal Cells

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

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

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

How Does Cancer Develop?

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

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

Genetic changes that cause cancer can happen because:

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

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

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

Fundamentals of Cancer

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

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

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

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

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

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

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

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

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

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

Types of Genes that Cause Cancer

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

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

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

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

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

When Cancer Spreads

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.

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AP®︎/College Biology

Course: ap®︎/college biology > unit 4.

Cell cycle control
Cell cycle checkpoints
Cell cycle regulators
Loss of cell cycle control in cancer

Cancer and the cell cycle

Regulation of cell cycle

Introduction

What’s wrong with cancer cells.

Normal cells in a culture dish will not divide without the addition of growth factors.
Cancer cells in a culture dish will divide whether growth factors are provided or not.
A normal cell with unfixable DNA damaged will undergo apoptosis.
A cancer cell with unfixable DNA damage will not undergo apoptosis and will instead continue dividing.

How cancer develops

Cell cycle regulators and cancer, tumor suppressors.

Two spontaneous mutations affecting the two different alleles may occur in the same cell over time.
A person may inherit one "bad" allele of the tumor suppressor from a parent, then lose activity of the other allele through a spontaneous mutation.

Check your understanding: viruses and cancer

(Choice A) E6 activates p53 A E6 activates p53
(Choice B) E6 makes p53 bind DNA more strongly B E6 makes p53 bind DNA more strongly
(Choice C) E6 triggers apoptosis through p53 C E6 triggers apoptosis through p53
(Choice D) E6 marks p53 for degradation (destruction) D E6 marks p53 for degradation (destruction)
If E6 made p53 more active, caused it to bind DNA more strongly, or triggered apoptosis, these changes would tend to decrease the chances of cancer development.
In contrast, if E6 marked p53 for degradation, p53 activity would decrease (because protein levels would be low) and the chances of uncontrolled cell division would increase, potentially leading to cancer.

Attribution:

Works cited:.

Hanahan, D. and Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell , 144 (5), 647. http://dx.doi.org/10.1016/j.cell.2011.02.013.647
Hanahan, D. and Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell , 144 (5), 649. http://dx.doi.org/10.1016/j.cell.2011.02.013 .
Bartlett, Zane. (2014, November 14). The Hayflick limit. In The Embryo Project Encyclopedia . Retrieved from https://embryo.asu.edu/pages/hayflick-limit .
Hanahan, D. and Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell , 144 (5), 651. http://dx.doi.org/10.1016/j.cell.2011.02.013.647
Hanahan, D. and Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell , 144 (5), 647, 659-660. http://dx.doi.org/10.1016/j.cell.2011.02.013.647
Vogelstein, B. and Kinzler, K. W. (2004). Cancer genes and the pathways they control. Nature Medicine , 10 , 790. http://dx.doi.org/10.1038/nm1087 .
Reece, J. B., Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., and Jackson, R. B. (2011). The cell cycle. In Campbell biology (10th ed.). San Francisco, CA: Pearson, 247
Vogelstein, B. and Kinzler, K. W. (2004). Cancer genes and the pathways they control. Nature Medicine , 10 , 789. http://dx.doi.org/10.1038/nm1087 .
Hanahan, D. and Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell , 144 (5), 658. http://dx.doi.org/10.1016/j.cell.2011.02.013.647
Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., and Darnell, J. (2000). Proto-oncogenes and tumor suppressor genes. Molecular cell biology (4th ed., section 24.2). New York, NY: W. H. Freeman. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK21662/#_A7092_ .
Roberts, P. J. and Der, C. J. (2007). Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer. Oncogene , 26 , 3292. http://dx.doi.org/10.1038/sj.onc.1210422 .
Santarpia, L., Lippman, S. L., and El-Naggar, A. K. (2012). Targeting the mitogen-activated protein kinase RAS-RAF signaling pathway in cancer therapy. Expert Opin. Ther. Targets 16 (1), 103-119. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3457779/#S6title .
Raven, P. H., Johnson, G. B., Mason, K. A., Losos, J. B., and Singer, S. R. (2014). Cancer is a failure of cell cycle control. In Biology (10th ed., AP ed., pp. 202-204). New York, NY: McGraw-Hill.
Vogelstein, B., Sur, S. & Prives, C. (2010). p53: the most frequently altered gene in human cancers. Nature Education , 3 . Retrieved from http://www.nature.com/scitable/topicpage/p53-the-most-frequently-altered-gene-in-14192717 .
Vogelstein, B., Lane, D., and Levine, A.J. (2000). Surfing the p53 network. Nature , 408 , 307-310. http://dx.doi.org/10.1038/35042675 .

Additional references:

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What Is Cancer?

PMID: 31761807
DOI: 10.1353/pbm.2019.0046

This essay focuses on themes in Explaining Cancer: Finding Order in Disorder (2018) by Anya Plutynski, a monograph that has important things to say about both the peculiarities of cancers and our theories about them. Cancer's agents of destruction are human cells that have been recruited and to some extent transformed into pathological organisms or the building blocks of tumors. Cancers both undermine and exploit mechanisms of multicellular organization, and understanding them gives rise to difficult philosophical problems. In addition to sketching Plutynski's discussion of these problems, this essay defends Christopher Boorse's account of disease from Plutynski's criticisms, and it expresses some qualms about her treatment of scientific explanation.

Neoplasms / etiology*
Philosophy, Medical

Essay on Cancer for Students and Children

500+ words essay on cancer.

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

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

Types of Cancers

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

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

Get the huge list of more than 500 Essay Topics and Ideas

Causes of Cancer

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

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

Treatment of Cancer

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

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

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Essay on Cancer

List of essays on cancer, essay on cancer – introduction, types and conclusion (essay 1 – 150 words), essay on cancer (essay 2 – 250 words), essay on cancer – for school students (essay 3 – 300 words), essay on cancer – for medical students (essay 4 – 400 words), essay on cancer – for science students (essay 5 – 500 words), essay on cancer (essay 6 – 600 words), essay on cancer – written in english (essay 7 – 750 words), essay on cancer – for ias, civil services, upsc, ips and other competitive exams (essay 8 – 1000 words).

Cancer is a disease which is related to the abnormal growth of cells in a particular part of the body. Since the last decade, cancer has become one of the most feared diseases of all times, particularly due to the difficult treatment one has to undergo and the limitations of the treatment in curing this disease during later stages of cancer.

Audience: The below given essays are exclusively written for school and college students. Furthermore, those students preparing for IAS, IPS, UPSC, Civil Services and other competitive exams can also increase their knowledge by studying these essays.

Introduction:

Cancer is a group of more than 100 diseases that can develop in almost anywhere in the body. Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.

Types of Cancer:

There are various types of cancer. They include:

1] Breast cancer: This is type of cancer that forms in the cells of the breast.

2] Prostate cancer: This is type of cancer that occurs in a man’s prostate. This is a small walnut sized gland that has the duty of producing seminal fluid.

3] Lung cancer: This is a type of cancer that begins in the lungs and this occurs mostly in people who smoke.

4] Leukemia: A cancer of blood forming tissues, hindering the body’s ability to fight infection.

Conclusion:

We have seen various types of cancer but the types of cancer we have are hundreds but we had mentioned just a few. Each type of cancer comes with various symptoms and various ways of curbing it.

Cancer is a disease that has been around for centuries, but it has never had such an impact on public health as it has now. Cancer is the increase in the number of cells in human beings at an abnormal rate. Doctors have been discussing the reasons behind this increase for the past fifty years. One is tempted to think that there are no reasons behind this occurrence and that it is just a natural phenomenon, people die all the time. Right?

The thing is that the number of cancer cases has increased in the past decades and a lot of this increase is attributed to the influence of different types of radiation. Even though most of the really dangerous substances (or sources of radiation) are not allowed near people. What else can be causing such an increase in cancer cases?

Some doctors have made a discovery regarding cancer that can really help us get rid of this problem. Following down the line of the argumentation presented in the famous “China Study” more doctors are advising their patients to change their diet because it can help in their fight against cancer. Not only that but a proper diet can also be the best prevention.

When you are a student your metabolism is young so you do not feel the bad effect of your habits as much as older people do but as we age the side effects of our bad choices will become obvious. We can teach ourselves to listen to our bodies and to prevent cancer but to do that we, first of all, have to defeat our habits.

Cancer is uncontrolled and unchecked development of abnormal cells in a part of the body. Cancerous cells develop just like another cell in the body. They, however, keep growing and can form a mass then subsequently becomes tumors. Since cells are present in every part of our body, cancer can also grow in all parts of our body.

Causes of Cancer:

One great scientific mystery in our world is the cause of cancer. Scientists from all over have tried and failed in isolating any particular action, substance or environmental factors that can lead to cancer.

However, scientists all over the world agree that cancer is caused by substances known as carcinogens. These substances are introduced to the body when we are exposed to or consume materials containing them. One of the confirmed sources of carcinogens is exposure to radiation from x-ray machines.

Cancer Treatment:

There are various ways to treat a person infected with cancer. These modes of treatment are chosen depending on the type of cancer, the stage of development and the health peculiarities of the cancer patient. In other cases, several modes of treatment are combined to treat a single patient.

Some of the modes of treating cancer are in fly highlighted below:

1. Surgery to remove Cancerous tumors from the body.

2. Radiation therapy to reduce the growth of cells.

3. Chemotherapy for destroying cancer cells.

4. Stem cell transplant.

Prevention of Cancer:

Just as there are no agreed actions, materials and exposure that causes cancer, there are no generally accepted means of preventing cancer. However, there are certain habits that can limit a person’s exposure.

Some of them are highlighted below:

1. Healthy environment and diet.

2. Reduction of exposure from the sun.

3. Keep your weight low.

4. Avoid the use of tobacco.

Early detection of cancer has been hailed as the most potent way of treating this menace. Though scientists are still in the business of searching for a cure, we as humans can prevent cancer by regular medical check-ups.

Cancer is one of the second largest fatal illnesses across the world. One of the horrific words a human being can listen to is being diagnosed with Cancer. The word Cancer brings alarm and anxiety to the listener. Cancer is the abnormal growth of cells in one part of the body which can even spread to other parts if not treated at an early stage. Neoplasms or tumour are the subset of these abnormally grown-up cells which often results in a mass or lump.

What causes Cancer?

Those agents which cause cancer are termed as Carcinogens . These can be classified into physical, chemical and biological. Physical Carcinogens include ultra violet and other ionizing radiations. Food adulterants such as aflatoxin, tobacco smoke, drinking water contaminant such as Arsenic, asbestos etc., are termed as Chemical Carcinogens. Viruses, Bacteria and other parasites which cause infections and eventually lead to Cancer are categorized under Biological Carcinogens. Ageing also causes cancer as the risk of the cellular repair mechanism weakens as we age.

Significant Symptoms of Cancer:

Some of the major symptoms of cancer include unexplained weight loss, extreme fatigue, persistent sores that do not heal, changes in the bladder and bowel movements, odd bleeding and discharges, change in voice due to cancer indication in larynx and lumps and bumps on the skin.

Preventive Measures:

Some of the risk factors which needs to be addressed to prevent cancer may include avoidance of tobacco, being overweight or obese, unhealthy eating with less vegetables and greens, physical in-activity, avoiding pollution etc. Apart from the mentioned, vaccination against HPV and Hepatitis B Virus, controlling hazards while at work, reducing exposure to ultra violet and ionizing radiation etc., can help prevent being infected by Cancer.

Assessing the type of cancer and the stage is very important because every cancer type has a different pattern of treatment from surgery, radiotherapy and chemotherapy . The treatment that is used to relieve the cancer patient from their pain and enhance the quality of life for the patients and their families is termed as Palliative care.

World Health Organization has partnered with UNO and other non-profit organizations to ensure every country is being made aware of the non-communicable diseases and the prevention of cancer and its control. Insights to develop Centers of Excellence to provide quality treatments and to conduct research on the carcinogenesis should be provided to governments and to help the people.

The abnormal cell growth in our body which spreads to other parts as well is what is termed as cancer. Around four lakh of people in India are known to be affected by this disease every year. More so, around half of them are not able to survive as they are usually detected in the last stages of cancer. Hence it is all the more important to educate the people about this disease and its symptoms so that it can be detected early and the lives of the people suffering from it can be saved.

Cancer can affect any body part. The part that is affected gives it the name, for instance, lung cancer which affects the lungs, skin cancer in which the skin is affected and so on. However, we can broadly divide cancer into four types. The first one is Sarcoma which is known to affect the blood vessels, bones, muscles cartilages and connective tissues. The second type of cancer is Carcinoma which affects the internal organs of the body or the skin. The third type is the Lymphoma. This cancer affects the lymph glands and the lymph nodes. The last type in which cancer can be categorised is Leukaemia which largely affects the parts forming blood such as the bone marrow.

Symptoms of Cancer:

Although no particular cause is known to trigger this disease, some activities have been associated as the cause of different types of cancer. The first and foremost is smoking. Excess smoking affects the entire respiratory system thereby leading to the onset of lung cancer. More so chewing tobacco is also attributed to giving rise to mouth and throat cancer. Similarly, alcohol is attributed to be the cause of stomach, liver and gallbladder cancer. Summarising it, all the ill habits of society and urbanisation have been attributed to this disease. Even radiations coming from X-ray machines can prove harmful and lead to cancer. That is why there are proper laws an protection in place when exposing people to these harmful radiations.

Treatments Available:

If detected in early stages, cancer can surely be curable. Surgery is one of the primary steps of curing this disease. If required, doctors remove the body part affected such as the uterus, gallbladder or the breast. Thereafter, through radiotherapy, the cancerous cells on the other affected parts of the body are killed so that they don’t spread to other parts. Chemotherapy is done using the strong chemical in order to kill the cancerous cells. Other methods such as tumour suppressing genes are used in different types of cancer as may be the need advised by the doctors. Whatever the method, it is extremely difficult to go through the pain and social stigma such as loss hair which comes alongside the treatment of cancer.

Living with this Disease:

It is indeed very difficult to live with this disease as not only this disease is not fully curable but the treatment is so tough that it scares even the toughest of individuals. We, as a society, must support the people suffering from cancer and help in their difficult times. We must not discriminate them and must understand that is already suffering a lot and must not do anything which further aggravates their sufferings.

Cancer is a severe disease in which there is abnormal growth of cell that spreads around the human body. Many people in the world are struggling with this disease. Consistently around 10 million cases are analyzed. These number of cases are expected to increase around 20 million by 2020. It turns into the most widely recognized reasons for death. Due to abnormal cell growth, it develops & affects the overall body weight. Prolonged cough and abnormal bleeding are some symptoms of this severe disease. The developed abnormal cells first make their impact on organs then slowly moved as poison. Cancer disease can be identified in the beginning periods. The medical professionals are still trying to catch this disease.

One of the main causes of cancer is smoking. Other causes include tobacco, consumption of alcohol, obesity, lack of physical activities, exposure to UV radiations, etc. Age factor and changes in genes are yet other factors that cause cancer.

Cancer has different types which can be divided into various forms:

i. Skin Cancer:

It is the most common type of cancer which can be seen in many people. Every year more than 1 million people are affected by skin cancer. Skin cancer happens due to the overexposure from the sun. The thicker ozone layers directly harms our skin, which increases the chances of skin cancer.

ii. Lung Cancer:

This type of cancer is related to the cells inside the lungs. The symptoms of this type of cancer are chest pain & sudden weight loss. It is also known as lung carcinoma. As a process of metastasis, the growth of abnormal cell growth spread inside the lungs. Smoking is a fundamental driver of Lung cases.

iii. Kidney Cancer:

Another name of kidney cancer is renal cancer. Renal Cell Carcinoma and Transitional Cell Carcinoma are the types of kidney cancer. This development of cancer happens after the age of 40 years. Smoking can twofold the danger of kidney malignant growth.

iv. Leukemia:

This cancer starts developing in the bone marrow, which leads to a high number of abnormal white cells. Acute myeloid leukemia or acute lymphocytic leukemia are the sorts of leukemia. Chemotherapy or radiation therapy can be used as the treatment for Leukemia.

Cancer Staging:

It is important to understand the staging factor of this severe disease. Diagnosis of cancer in early stages helps to tackle this disease by proper treatments. During the initial stages of cancer, proper surgeries or radiotherapy can help to overcome cancer. When the broken cancer cells move to other parts of the human body, then advance treatment is suggested by the professionals. But when a patient is in the final stages of cancer, he needs a treatment which covers his whole body. Chemotherapy is a therapy which is used to circulate the bloodstream. Professional doctors use various test techniques to identify the stages of cancer. Stages are used to describe the severity of cancer.

In the initial stage, cancer can be prevented through medication, proper surgeries and light treatment. In the advance stages of cancer, chemotherapy and radiation therapy is useful. Above all, the best way to keep cancer away is to stay away from smoking and tobacco, eat healthy food and a lot of green vegetables, and do some physical exercise daily.

It is very difficult for a cancer patient to fight with the final stages of cancer. To deal with this severe problem cancer symptoms should never be ignored. More than 70% of cases are seen only due to smoking. At every stage, it is essential that everyone must adopt a healthy diet plan & exercise daily to prevent this disease. A person who has a good and healthy lifestyle can fight with cancer more strongly.

Current trends in global health mention cancer. Cancer is currently one of the leading causes of death globally. It is an illness in which abnormal cell growth develops and affects parts of the human body as it advances, it has the potential to spread from one part of the body to the other. It is a chronic illness that imposes a great economic burden on a nation because its management is costly. Cancer occurs in different parts of the body and are classified according to where it has affected. In India, men are mostly acted by lung, oral, lip and neck cancers whereas women are affected by cervical, breast and ovarian cancer. The detection procedure varies with the type of cancer while the treatment varies with the stage of the cancer progression. Mostly early stages of cancer have better prognosis compared to late stages of cancer.

There are modifiable and non-modifiable factors that predispose an individual to cancer. Non modifiable factors include age and genetics. With an increase in age, the rate of cancer incidence increases. The genetic predisposition to cancer increases the incidences of suffering the disease. Modifiable factors include lifestyle habits like drinking and smoking tobacco which increase the incidences of lung, oral, esophageal among other cancers. Diet is also a predisposing factor especially one that is less in vitamin supplements.

Physical inactivity and obesity predispose to cancers of the colon, breast and others. Sexual activity in women with multiple sexual partners predisposes them to cervical cancer due to the transmission of HPV (Human Papilloma Virus). The environment also predisposes to cancer because of the chemicals, radicals and radiations that interact with human beings.

Detection of Cancer:

The detection varies with the type of cancer and so screening is done for each type differently. It is advisable that people get regular checkups of the whole body so that early detection facilitates effective and curative treatment. Screening of cancer is done using detailed examination of the physique, laboratory and histology tests, radiological and magnetic imaging techniques among other methods.

The campaigns against cancer advocate for early detection by teaching the public on the early signs of cancer. In breast cancer awareness for example, the public is made aware of physical examination of the breast and if they detect any abnormal growth or lump, they are to seek further investigation. Early detection is important because it results in successful treatment. In the detection, the cancer staging is done, which is usually four stages, stage one, two, three and four. Stage one has the best prognosis whereas stage four has the poorest prognosis.

Treatment of Cancer:

Once cancer is detected, a range of treatment options is provided. Treatment depends on the types of cancer and the staging. It can be treated by surgery whereby excision of the abnormal growth is done. Surgery is done for non-hematological cancers and those that have not metastasized to other parts of the body. An example of surgery is mastectomy to treat breast cancer.

Chemotherapy is another treatment option that involves the administration of anticancer medication that eliminate the abnormal cells in the body. Another treatment option is radiation therapy that uses ionizing radiations to destroy cancer cells. Radiation is also used to make tumors small. It is used to treat solid tumors and it depends on the sensitivity of the tumor to the radiations. It is targeted at the nucleic acid destruction in the tumor cells.

Consequences of Cancer:

Cancer is a chronic illness that could result in very serious consequences even with treatment. Cachexia is the extreme wasting of the body that causes death in cancer patients. Economic burden to both the individual and the nation is experienced in cancer treatment because the treatment modalities are costly. The economic burden results in decline of the nation’s economy and increased healthcare costs to the population.

Mental illnesses result from cancer because it is a terminal illness and most patients become mentally unstable upon diagnosis. The quality of health is affected in a country when there is high incidences of cancer and the performance is greatly affected, which cause poverty and economic crisis for individuals.

Cancer is a serious illness that impacts the lives of people and the nation negatively. It is evident that cancer has diverse treatment options but the problem is that people do not go for checkups. Checkups are important in early detection, which usually results in successful treatment and less burden of cancer in a nation and in individuals.

Cancer is basically an agglomeration of various diseases that involves the abnormal growth of cells with the ability to spread or invade other body parts. Cancers are quite different from benign tumours in that the latter does not spread or invade other body parts. Some of the many symptoms and signs of cancer include abnormal bleeding, a lump, weight loss that is unusual, prolonged cough and bowel movement change. Even though these listed symptoms and signs of cancer, they might be caused by other things so it is necessary to be diagnosed. Today, we have more than 100 various kinds of cancer that affect us humans.

History of Cancer:

It is believed that cancer has been in existence for a majority if not all of the history of man. Breast cancer was the first form of cancer that was recorded and this happened around 1600 BC in Egypt. Between 460 BC and 370 BC, Hippocrates spent time analysing various types of cancer and referred to them as crayfish or crab. The name was as a result of the crab-like look of the malignant tumour and the lateral extension of the distended veins and tumours.

Factors Causing Cancer:

It has been discovered that the major cause of deaths as a result of cancer is the use of tobacco and it accounts for about 22 percent of the total number of deaths due to cancer. Poor diet, obesity, excessive alcohol consumption and a lack of exercise and physical activities accounts for another 10 percent of deaths caused by cancer. Some other causes and factors that contribute to cancer include environmental pollutants, ionizing radiation exposure and certain infections.

In most developing countries, infections like hepatitis B, Helicobacter pylori, papillomavirus infection of humans, Hepatitis C, HIV and Epstein Barr contribute to fifteen percent of all cancers. All of the factors listed above change the cell genes. There are always a lot of genetic changes before the development of cancer. About 10% of all cancers are as a result of genetic defects that are inherited from a parent. Asides the symptoms and signs that are used to detect cancer, screening tests are also a good way of detecting cancer. Cancer is normally thoroughly investigated using medical imaging; it is then confirmed through biopsy.

Development of Cancer:

A tumour or neoplasm is a collection of cells which have gone through growth that is not regulated and most times form a lump or mass. Every tumour cell exhibits the six important characters that are necessary for the production of the malignant tumour.

The six characteristics are:

1. Cell division and growth without all the signals that are proper.

2. Continuous division and growth even though the signals given are contrary.

3. Cell death that is usually programmed is avoided.

4. The divisions of the cell are quite limitless in number.

5. The construction of blood vessel is promoted.

6. The tissues are invaded and metastases are formed.

Cancer Prevention:

The prevention of a lot of cancers can be ensured by trying to maintain a weight that is healthy, not smoking, consuming a lot of whole grains, fruits and vegetable, avoiding the consumption of a lot of alcohol, reduction in the amount of red and processed meat that is consumed, getting vaccinated against some infectious diseases and the avoidance of too much exposure to sunlight. It is sometimes useful that there is early detection in cases of colorectal and cervical cancer and this can be achieved through screening. The usefulness of breast cancer screening is highly controversial.

The treatment of cancer is usually done by combining surgery, radiation therapy, targeted therapy and chemotherapy. A very important element of care is the management of symptoms and pain. In cases of advanced disease, palliative care is of utmost importance. The extent of the disease at the commencement of treatment and also the form of cancer that is involved go a long way to determine the odds of survival. Using the adopted survival rate at five years, children that were under the age of 15 when they were diagnosed have an average rate of survival of 80% in most developed countries. In the US, the average rate of survival for the five year period is 66%.

90.5 million people were living with different cancers in 2015. It has been reported that every year, close to 15 million reports of new cancer cases are filed. These do not include the cases of skin cancer. Cancer results in more than eight million deaths every year which is about 15.7% of the total number of deaths every year.

In males, prostate cancer, lung cancer, stomach cancer and colorectal cancer are the most widespread cancer types. In females, colorectal cancer, breast cancer, cervical cancer and lung cancer are the most widespread cancer types. Apart from melanoma, if we include skin cancer in the amount of new cases of cancer every year, it is going to be 40% of the total number of cases.

Brain tumours and lymphoblastic leukemia that is acute are the most widespread cancer types in children but in Africa, lymphoma that is no-Hodgkin is the most widespread. The total number of children that are under the age of 15 that ended up being diagnosed with one type of cancer or the other in 2012 is around 165,000.

With an increase in age, it has been seen that the risk of getting cancer also increases significantly and the number and occurrence of cases of cancer in developed countries in more than the number and occurrence of cancer cases in other countries. The change in lifestyle and increase in the number of people living to a very old age in countries that are developing contributes to the increase in the rate of the occurrence of cancer. Cancer is believed to have a financial cost of up to 1.16 trillion dollars every year.

Cancer can be extremely dangerous when it is not discovered early and when adequate and proper care and attention is not given to the treatment. Therefore it is very important to go for regularly screening to find out if there is need for caution or treatment.

Cancer , Diseases , Health

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Home — Essay Samples — Nursing & Health — Cancer — Cancer And The Process Of Cell Division

Cancer and The Process of Cell Division

Categories: Cancer

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Published: Feb 8, 2022

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Introduction, the cell cycle, cell division, cell growth, cancer treatment.

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Leukemia: Causes, Pathogenesis, Morphological Changes, Basic Management Studies are ongoing to establish the exact cause of the disease, which is still unknown according to the Leukemia and Lymphoma Society.
MD Anderson Cancer Center: Community Health Assessment The focus of the assessment is the city of Houston, Texas, and the MD Anderson Cancer Center. Most health issues are related to income disparities, immigration status, and the insurance status of Houston residents.
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Local Inflammation and Human Papillomavirus Status of Head and Neck Cancers The objective of the study was to assess whether periodontitis is related to the human papillomavirus status of the head and neck squamous cell carcinoma.
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Community Nursing Role in Breast Cancer Prevention However, early detection still remains important in the prevention and treatment of breast cancer. The community has thus undertaken activities aimed at funding the awareness, treatment and research in order to reduce the number of […]
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Measuring the Uncertainty in Children With Cancer The Limitations of using Mishel Uncertainty Illness Scale and Children Uncertainty Illness Scale led to the development of Uncertainty scale for kids.
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Prognosis in Ulcerative Colitis for Risk of Cancer After that the attempt was to extract the information about incidence of colon cancer in populations previously diagnosed with ulcerative colitis, to check whether the cancer risk increased with the duration of disease and finally […]
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Nutritional Assessment for Cancer Patients The consumption of fatty fish and a reduction in the consumption of unhealthy fats can reduce the risk of colon cancer that is brought about by the consumption of animal fat.
Cancer Treatment Measures in the Sydney Cancer Center Overall, the study enhanced the proper understanding of the effectiveness through the analysis of the number of health specialists working in the Sydney Cancer Centre and the number of cancer patients attended per day.
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Sonodynamic Therapy for Cancer Treatment Sonodynamic therapy also known as ultrasound therapy is a hopeful innovative cancer treatment method that focuses on synergistic effect on tumor cell killing of a photosensitizer and ultrasound. Cavitation refers to the growth, oscillation and […]
The Relationship Between Cancer and Lifestyle In addition, other lifestyle aspects, such as cigarette smoking, sun exposure and stress need to be addressed to reduce the risks of cancer.
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Effects of Hypoxia, Surrounding Fibroblasts, and p16 Expression on Breast Cancer The study was conducted to determine whether migration and invasion of breast cancer cells were stimulated by hypoxia, as well as determining whether the expression of p16 ectopically had the potential to modulate the cell […]
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The Effective Pain Assessment in Patients With Lung Cancer
Providers’ Role in Quality Assurance in Breast Cancer Screening
Framing Qualitative Research on Lung Cancer
Oncology: Colorectal Cancer
Prostate Cancer: Symptoms and Treatment
Clinical Laboratory Science of Breast Cancer
Induced and Spontaneous Abortion and Breast Cancer Incidence Among Young Women
Quality of Life in Chronic Leukemia Patients
Dyspnea in Cancer Patients
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Lung Cancer Cells Migrating to Other Parts of the Body
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To Live Until You Die: Palliative Care in Cancer Experience
Care Needs of Children Whose Parents Have Incurable Cancer
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Breast Cancer in Afro- and Euro-Americans
Cancer Treatment and Life Quality in Adult Patients
Breast Cancer Assessment in London
Oral Cancer Reconstruction
Skin Cancer Awareness Overview
Angiostatic Approaches to Cancer Therapy
Genetics of Prostate Cancer and Physical Features
Epithelial Ovarian Cancer Investigation
Creativity in People With Cancer
Cancer: Alternative and Complementary Therapies
Promotion of Cardiovascular Health and Cancer Prevention
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Cancer Longitudinal Exploration
Breast Cancer: At-Risk Population, Barriers, and Improvement
Effective Solutions to the Prevention of Cervical Cancer
Breast Cancer: Moral and Medical Aspects
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Breast Cancer Risk Factors: Genetic and Nutritional Influences
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The Role Genetics Information Plays in Treating Cancer
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Leukemia Types: Characteristics, Genetics, and Symptoms
CRISPR and Cas-9 Technology as the Solution to Cancer
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World Health Organization Cancer Website Tool
Long Distance Cancer Treatment Ethics
A Community Capacity-Enhancement Approach to Breast and Cervical Cancer Screening
The Role of Inflammation in Cancer
Cognitive Behavioral Therapy: Plan for Cancer Pain
Psychosocial Factors & Immune Mechanisms in Cancer Regulation
Fundraising Methods for the Canadian Cancer Society
Nutrition and Cancer Rates
Breast Cancer Diagnosis Procedure in Saudi Arabia
Language and Stigmatization: Cancer, HIV, and AIDS
The Three Most Common Types of Cancer in America
Breast Cancer and the Effects of Diet
J. Overcash on Older Adults With Cancer
Postmenopause Hormone Therapy and Endometrial Cancer
Risk Factors for Cervical Cancer
When the Smoke Clears: The Story About the Lung Cancer
Motivational Interviewing as a Smoking Cessation Intervention for Patients With Cancer
Genetic Predisposition to Breast Cancer: Genetic Testing
Cancer Pathophysiology and Nursing Management
Breast Cancer: Causes and Treatment
Integumentary System Diseases. Skin Cancer and Eczema
Digestive Cancer. Complementary & Alternative Treatment
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Ethics of Leukemia Treatment With Disabled HIV Cells
Human Papillomavirus Infection and Cervical Cancer
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Penectomy Challenges in Cancer Patients
Monoclonal Antibodies in Treating Breast Cancer
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Breast Cancer Screening in Young American Women
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Children With Cancer and Their Social Activities
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Screening for Breast Cancer
The Role of Epigenetics in Cancer: Contributors to the Formation of Cancer Tumors
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Prostate Cancer and Age-Related Risk Factors
Gua Sha in Cancer Therapy Against Myalgia
Gastric Cancer Diagnosis and Treatment
Cervical Cancer and Risk Factors
Annual Breast Cancer Awareness Campaign
Cervical Cancer: Medical Imaging and Radiotherapy
Testicular Cancer: Diagnosis and Treatment
Organic Foods Consumption and Cancer Prevention
Prostate Cancer, Its Genetics and Prevention Methods
Cancer Epidemiology Among Chinese Americans
Colorectal Cancer, Diagnosis and Treatment Plan
Prostate Cancer Symptoms and Laboratory Tests
Skin Cancer in Australia and Health Campaign
Breast Cancer Patients’ Life Quality and Wellbeing
Obesity as a Risk Factor for Uterine Cancer
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Palliative Care for Adult Patients With Cancer
Breast Cancer Patients’ Functions and Suitable Jobs
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Cancer Patients’ Financial Status and Life Quality
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Cancer Disease and Its Impact
Breast Cancer Screening Among Non-Adherent Women
Healthcare Research: Bladder Cancer Independent Variables
Cancer Patient’s Autonomy and Medical Ethics
The Internet Use at MD Anderson Cancer Hospital
American Cancer Society’ Social Media Networks Usage
Breast Cancer: Treatment and Rehabilitation Options
The Effectiveness of Music for Cancer Patients
Women Healthcare: Breast Cancer
Skin Cancer: Types and Cells of Origin
Prevention of Cancer: Good Nutrition and Positive Behavior
Lung Cancer Disease and Prevention Methods
Breast Cancer Public Relations Campaign
Technologies: Improving the MD Anderson Cancer Center Website
Explanation of Cancer Disease
Gallbladder Cancer, Its Causes and Rates
Health Information Seeking and Breast Cancer Diagnosis
Stem Cell Therapy in Colorectal Cancer
Employing Cancer Vulnerability Reduction in Ukraine
Current Standing of Breast Cancer and Its Effects on the Society
Descriptive Epidemiology of Cancer in the UK
International Expansion Strategy of Australia Cancer Care Hospital.
American Cancer Society History
Medical Marijuana use for Terminal Colon Cancer
Asbestos and Rising of Cancer
The Problem of Skin Cancer in Australia
Health Outcome of Tobacco Use: Lung Cancer
Prostate Cancer Treatment
Breast Cancer: Disease Prevention
Breast Cancer Definition and Treatment
Breast Cancer Symptoms and Causes
Radiation Therapy for Testicular Cancer
Breast Cancer Incidence and Ethnicity
Treatment Options for Breast Cancer
Cancer Treatment by Nanotechnology
Health Risks and Prevention: Cardiovascular Disease and Cancers
Healthcare Demographics of Prostate Cancer in the US
Malevolence of Cancer: Pathogenesis and Treatment Options
Risk Factors, Staging, and Treatment of Breast Cancer
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10 April 2024

How to supercharge cancer-fighting cells: give them stem cell skills

Sara Reardon 0

Sara Reardon is a freelance journalist based in Bozeman, Montana.

You can also search for this author in PubMed Google Scholar

A CAR T cell (orange; artificially coloured) attacks a cancer cell (green). Credit: Eye Of Science/Science Photo Library

Bioengineered immune cells have been shown to attack and even cure cancer , but they tend to get exhausted if the fight goes on for a long time. Now, two separate research teams have found a way to rejuvenate these cells: make them more like stem cells .

Both teams found that the bespoke immune cells called CAR T cells gain new vigour if engineered to have high levels of a particular protein. These boosted CAR T cells have gene activity similar to that of stem cells and a renewed ability to fend off cancer . Both papers were published today in Nature 1 , 2 .

The papers “open a new avenue for engineering therapeutic T cells for cancer patients”, says Tuoqi Wu, an immunologist at the University of Texas Southwestern in Dallas who was not involved in the research.

Reviving exhausted cells

CAR T cells are made from the immune cells called T cells, which are isolated from the blood of person who is going to receive treatment for cancer or another disease. The cells are genetically modified to recognize and attack specific proteins — called chimeric antigen receptors (CARs) — on the surface of disease-causing cells and reinfused into the person being treated.

But keeping the cells active for long enough to eliminate cancer has proved challenging, especially in solid tumours such as those of the breast and lung. (CAR T cells have been more effective in treating leukaemia and other blood cancers.) So scientists are searching for better ways to help CAR T cells to multiply more quickly and last longer in the body.

Cutting-edge CAR-T cancer therapy is now made in India — at one-tenth the cost

With this goal in mind, a team led by immunologist Crystal Mackall at Stanford University in California and cell and gene therapy researcher Evan Weber at the University of Pennsylvania in Philadelphia compared samples of CAR T cells used to treat people with leukaemia 1 . In some of the recipients, the cancer had responded well to treatment; in others, it had not.

The researchers analysed the role of cellular proteins that regulate gene activity and serve as master switches in the T cells. They found a set of 41 genes that were more active in the CAR T cells associated with a good response to treatment than in cells associated with a poor response. All 41 genes seemed to be regulated by a master-switch protein called FOXO1.

The researchers then altered CAR T cells to make them produce more FOXO1 than usual. Gene activity in these cells began to look like that of T memory stem cells, which recognize cancer and respond to it quickly.

The researchers then injected the engineered cells into mice with various types of cancer. Extra FOXO1 made the CAR T cells better at reducing both solid tumours and blood cancers. The stem-cell-like cells shrank a mouse’s tumour more completely and lasted longer in the body than did standard CAR T cells.

Master-switch molecule

A separate team led by immunologists Phillip Darcy, Junyun Lai and Paul Beavis at Peter MacCallum Cancer Centre in Melbourne, Australia, reached the same conclusion with different methods 2 . Their team was examining the effect of IL-15, an immune-signalling molecule that is administered alongside CAR T cells in some clinical trials. IL-15 helps to switch T cells to a stem-like state, but the cells can get stuck there instead of maturing to fight cancer.

The team analysed gene activity in CAR T cells and found that IL-15 turned on genes associated with FOXO1. The researchers engineered CAR T cells to produce extra-high levels of FOXO1 and showed that they became more stem-like, but also reached maturity and fight cancer without becoming exhausted. “It’s the ideal situation,” Darcy says.

Stem-cell and genetic therapies make a healthy marriage

The team also found that extra-high levels of FOXO1 improved the CAR T cells’ metabolism, allowing them to last much longer when infused into mice. “We were surprised by the magnitude of the effect,” says Beavis.

Mackall says she was excited to see that FOXO1 worked the same way in mice and humans. “It means this is pretty fundamental,” she says.

Engineering CAR T cells that overexpress FOXO1 might be fairly simple to test in people with cancer, although Mackall says researchers will need to determine which people and types of cancer are most likely to respond well to rejuvenated cells. Darcy says that his team is already speaking with clinical researchers about testing FOXO1 in CAR T cells — trials that could start within two years.

And Weber points to an ongoing clinical trial in which people with leukaemia are receiving CAR T cells genetically engineered to produce unusually high levels of another master-switch protein called c-Jun, which also helps T cells avoid exhaustion. The trial’s results have not been released yet, but Mackall says she suspects the same system could be applied to FOXO1 and that overexpressing both proteins might make the cells even more powerful.

doi: https://doi.org/10.1038/d41586-024-01043-2

Doan, A. et al. Nature https://doi.org/10.1038/s41586-024-07300-8 (2024).

Article Google Scholar

Chan, J. D. et al. Nature https://doi.org/10.1038/s41586-024-07242-1 (2024).

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Scientists Discover How Cancer Creates 'Acid Wall' Against Immune System

S cientists have made a breakthrough discovery in our understanding of how cancer cells evade our immune systems. The findings, published in the journal Nature Biomedical Engineering , open new avenues for drug development in cancer research to better support our immune systems in killing cancer cells.

Cancer cells have three main ways of interacting with our immune systems: They can hide, fight back or erect a physical barrier. It is this third tactic that the team at University of Texas Southwestern has been investigating.

It has long been established that tumors are slightly more acidic than healthy body tissue. This is largely due to their production of lactic acid, a waste byproduct of the cells' metabolism. However, this acidity is not uniform across cancer cells.

In their latest study, Jinming Gao and his colleagues at UT Southwestern used nanoscale probes to measure how pH varies across tumor cells. They found that the cells were significantly more acidic on one side compared to the other. In other words, the acidity was polarized across the cells.

When similar tests were done on entire tumor tissues, the team found that the cancer cells pumped the acid away from their neighboring cancer cells and into the surrounding environment, creating a wall of increased acidity around the tumor's edge.

By studying samples from human tumor tissue, the team found that this wall of increased acidity was more or less devoid of the killer T cells our bodies rely on to fight off infections and other harmful cell types. In other words, the cancer was able to create an acid wall to protect itself from the immune system.

"This study revealed a previously unrecognized polarized extracellular acidity that is prevalent around cancer cells," Gao said in a statement.

These results have implications for the development of anti-cancer drugs. To start with, understanding the acidity of the environment surrounding cancer cells could help in the development of targeted cancer treatments that can be directed to the site of a tumor to deposit their active ingredients. In this case, the increased acidity can be used as a signal for the cancerous tissue to ensure the drug is delivered only to the site of the tumor.

As we develop our understanding of this process, we may also be able to design drugs to prevent cancer cells from producing acid walls, thus making them more vulnerable to attack from the immune system.

Is there a health problem that's worrying you? Do you have a question about cancer? Let us know via [email protected]. We can ask experts for advice, and your story could be featured on Newsweek .

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Artist's impression of killer T cells attacking a cancerous tumor. However, according to new research, tumors can produce an acid wall to protect themselves from the activity of our immune system.

Bacteria in cancer unmasked

Detailed catalogue of bacteria living in cancer metastases.

Researchers at the Netherlands Cancer Institute have compiled a detailed catalogue of bacteria living in cancer metastases. Having analyzed over 4000 tumors, they shed light on the diversity of these co-inhabitants and how they might interact with cancer cells and their surroundings. For example, certain bacteria were linked to a worse response to immunotherapy. This study paves the way to a better understanding of how bacteria help or hinder cancer (therapy), and how we can use this for patients' advantage. The researchers publish their findings today in the scientific journal Cell .

On and in our bodies live billions of microorganisms: bacteria, viruses and yeasts -- our microbiome. We need them, and they need us. Bacteria help us digest our food, for example, and cooperate with our immune system in the fight against pathogens. Gut bacteria in particular have been extensively studied, including in the context of cancer. For example, they can influence the effectiveness of immunotherapy and chemotherapy.

But these tiny co-inhabitants also house outside the gut. Bacteria are found in tumors, for example. With new techniques, researchers are getting better at finding out which microbes they are. But how bacteria get to a tumor and what exactly they do there remains largely unknown, making it unclear how important they are to disease and the effect of treatments.

26 cancer types

Because many patients eventually die from metastases, and many treatments target them, the research groups of Emile Voest and Lodewyk Wessels took a closer look at those metastases. After all, little was known about bacteria in these tumors. Together with their colleagues at, among others, the Netherlands Cancer Institute and Oncode Institute they have now mapped which bacteria are present in cancer metastases. Both groups are

In tissue from more than 4,000 metastases of 26 types of cancer, the researchers analyzed the code of the DNA present. From that genetic material you can see not only which human cells are there, but also which bacteria -- because these also have DNA. For this purpose they used clinical information and DNA data generated by Hartwig Medical Foundation.

With that unimaginably large mountain of information (400 terabytes), they used computer power to figure out which bacteria congregate in which places. This required a lot of clever programming, because there is relatively little bacterial DNA in such a piece of tissue.

"Surprisingly, it's not just metastases from colon cancer that contain a lot of bacteria," says researcher Thomas Battaglia. One might expect that because most of our bacteria reside in the colon, from where they could possibly travel along during metastasis to elsewhere in the body. "Also, which bacteria are present in a metastasis is strongly related to the location in the body, the conditions there, and the cancer type."

Therapy response

They also discovered a link between bacteria and therapy efficacy. Patients with lung cancer and Fusobacterium in their metastasis, for example, responded worse to immunotherapy than peers without that bacteria. Thomas: "We also noted that the more diverse the bacterial community, the more active the adjacent tumor cells."

"Our work opens doors for exploring new forms of treatments, for example against bacteria that might help the tumor," co-author Iris Mimpen says. "It helps us understand how the complex environment of tumors works, an environment in which all kinds of cells -- including bacteria -- live together and influence each other."

This research was financially supported by the AVL Foundation , KWF Dutch Cancer Society and Oncode Institute .

Brain Tumor
Colon Cancer
Lung Cancer
Microbiology
Microbes and More
Extreme Survival
Immune system
Prostate cancer
Cervical cancer
Colorectal cancer
Breast cancer
Esophageal cancer

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Materials provided by Netherlands Cancer Institute . Note: Content may be edited for style and length.

Journal Reference :

Thomas W. Battaglia, Iris L. Mimpen, Joleen J.H. Traets, Arne van Hoeck, Laurien J. Zeverijn, Birgit S. Geurts, Gijs F. de Wit, Michaël Noë, Ingrid Hofland, Joris L. Vos, Sten Cornelissen, Maartje Alkemade, Annegien Broeks, Charlotte L. Zuur, Edwin Cuppen, Lodewyk Wessels, Joris van de Haar, Emile Voest. A pan-cancer analysis of the microbiome in metastatic cancer . Cell , 2024; DOI: 10.1016/j.cell.2024.03.021

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Cancer and Aging: Two Tightly Interconnected Biological Processes

Lieze berben.

1 Laboratory of Experimental Oncology, Department of Oncology, KU Leuven, 3000 Leuven, Belgium; [email protected]

Giuseppe Floris

2 Department of Pathology, University Hospitals Leuven, 3000 Leuven, Belgium; [email protected]

3 Laboratory of Translational Cell and Tissue Research, Department of Imaging and Pathology, KU Leuven, 3000 Leuven, Belgium

Hans Wildiers

4 Department of General Medical Oncology, University Hospitals Leuven, 3000 Leuven, Belgium

Sigrid Hatse

Simple summary.

As life expectancy is increasing, the older population is rapidly growing. However, older patients with cancer are still underrepresented in clinical trials, making treatment of these patients challenging for oncologists. Robust biomarkers that reflect the body’s biological age can be helpful to provide older patients with cancer with an optimal personalized treatment. However, to be able to identify such biomarkers, more in-depth research is needed in this underexplored population. In this review, we have put together the current knowledge concerning the mechanistic connections between aging and cancer, as well as aging biomarkers that could be useful in the field of geriatric oncology.

Age is one of the main risk factors of cancer; several biological changes linked with the aging process can explain this. As our population is progressively aging, the proportion of older patients with cancer is increasing significantly. Due to the heterogeneity of general health and functional status amongst older persons, treatment of cancer is a major challenge in this vulnerable population. Older patients often experience more side effects of anticancer treatments. Over-treatment should be avoided to ensure an optimal quality of life. On the other hand, under-treatment due to fear of toxicity is a frequent problem and can lead to an increased risk of relapse and worse survival. There is a delicate balance between benefits of therapy and risk of toxicity. Robust biomarkers that reflect the body’s biological age may aid in outlining optimal individual treatment regimens for older patients with cancer. In particular, the impact of age on systemic immunity and the tumor immune infiltrate should be considered, given the expanding role of immunotherapy in cancer treatment. In this review, we summarize current knowledge concerning the mechanistic connections between aging and cancer, as well as aging biomarkers that could be helpful in the field of geriatric oncology.

1. Introduction

As life expectancy has increased dramatically over the past decades, older persons represent a rapidly growing section of our population. This results in an increasing number of older patients with cancer as well. Moreover, as cancer and aging are closely interrelated, cancer incidence is higher in the older age categories compared younger age categories [ 1 , 2 ]. There are several factors associated with aging that could explain this. Firstly, there is an accumulation of oxidative stress and DNA damage over the years that is caused by a life-long exposure to endogenous metabolic insults (e.g., free radicals) and exogenous factors (e.g., UV irradiation, foods, etc.). This may eventually lead to cell transformation and tumor initiation. Secondly, senescent cells accumulate during the aging process and exhibit a senescence-associated secretory phenotype (SASP); this means that they secrete inflammatory mediators (e.g., interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-2, growth-regulated oncogene alpha (GROα), etc.) that may promote tumor growth by creating a tumorigenic environment [ 3 ]. Finally, a progressive decay of immune function occurs in older individuals, whereby an effective immune response against developing tumors may fail [ 4 ]. As the aging rate is unique, biological age of a person can differ from the chronological age and two people of the same calendar age can show a different biological aging profile. Consequently, one individual could tolerate more aggressive treatments than another individual of the same age could. In addition, chemotherapy by itself is also believed to accelerate the aging process, which may result in premature aging and frailty [ 5 ]. Additionally, more extensive and intensive research is needed to gain a better understanding of the impact of aging on tumor immunity. As aging has a substantial impact on the immune system, it could influence the effectiveness of the upcoming immunotherapies [ 6 , 7 , 8 ]. As for now, we do not have optimal tools available for estimating the “biological” age of patients, which is far more relevant than their chronological age.

Clinical decision-making in geriatric oncology is currently suboptimal, and many older individuals are under-treated while others are over-treated. Under-treatment may lead to increased risk of relapse and higher mortality while over-treatment can lead to a decreased quality of life due to toxicities [ 9 , 10 , 11 ]. There is thus an urgent need for better tools to select cancer patients for specific therapies. These tools should be prognostic, providing information on the patient’s life expectancy, and also predictive for the therapeutic benefit that will be achieved by the treatment. Aging biomarkers are promising candidate tools for this purpose, which definitely merit profound investigation in a clinical setting. Several candidate aging biomarkers have been described in the literature but to date, none of these have found their way from bench to bedside [ 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 ]. In this review, we discuss the interplay between aging and cancer based on the current literature, together with potential promising biomarkers that could be useful in geriatric oncology.

2. Mechanistic Interface between Aging and Cancer

Aging has been acknowledged as a major risk factor for developing cancer. Moreover, the two are highly interrelated and this is reflected by the numerous shared underlying mechanisms. The following three elements involved in the aging process, also play significant roles in cancer [ 25 , 26 , 27 ].

2.1. Cellular Damage and DNA Damage Response

Accumulation of cellular damage is probably the most important driver of both aging and cancer, and can be caused by several shared events. Life-long exposure to many endogenous (e.g., free radicals) and exogenous (e.g., UV radiation, foods, etc.) stress factors can induce an increase of oxidative stress, leading to genomic instability and ultimately DNA damage [ 25 , 26 , 27 ]. Reactive oxygen/nitrogen species can react with DNA and can cause several types of DNA damage such as oxidation of purines and pyrimidines, single strand breaks and double-strand breaks [ 28 , 29 ]. Antioxidant systems like antioxidant enzymes (i.e., catalase and glutathione peroxidase), vitamins (i.e., vitamins C and E) and other radical scavengers (glutathione) are able to prevent oxidative DNA damage. Yet, when this first line defense is ineffective, the DNA damage response is triggered and the cell cycle is arrested to allow DNA repair mechanisms to restore the damage ( Figure 1 ) [ 28 , 29 ]. Essential nonredundant players of the DNA damage response are ataxia-telangictasia-mutated (ATM), recruited after a double strand break via the DNA damage sensor complex MRE11-RAD50-NSB1, and ataxia-telangictasia-Rad3-related (ATR), induced after a single strand break detected by RPA, ATRIP or the RAD6-RAD1-HUS1 complex. In their turn, ATM and ATR activate several DNA damage mediators, such as breast cancer gene 1 (BRCA1) and downstream kinases like checkpoint kinases (CHK) 1 and 2. The latter are able to trigger effectors like P53, ensuring initiation of either apoptosis, cell cycle arrest or DNA repair [ 30 ]. The two most important mechanisms are base excision repair and nucleotide excision repair [ 28 , 29 ]. When the DNA repair mechanisms are also unsuccessful, either the apoptotic pathway or senescence program can be activated (as explained in more detail below in Section 2.2 ) to eliminate cell carrying potentially dangerous mutations that can lead to cell transformation and tumor initiation [ 25 , 26 , 27 , 28 , 29 ].

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Object name is cancers-13-01400-g001.jpg

Simple overview of the DNA damage response after oxidative DNA damage. Double strand breaks recruit ataxia-telangictasia-mutated (ATM), whereas single strand breaks induce ataxia-telangictasia-Rad3-related (ATR). DNA damage response mediators and downstream kinase can be activated whereby either DNA repair, apoptosis or cell cycle arrest will occur.

Besides direct DNA damage, telomere shortening has been shown to trigger a DNA damage response. Telomere length decreases with aging as telomeres shorten with each cell division. Short telomeres are associated with genomic instability, which occurs in early tumor development, and are a significant risk factor for aging-related diseases [ 25 , 26 , 27 ].

2.2. Cellular Senescence

Cellular senescence is considered to be one of the most important driving forces of the aging process [ 25 ]. It is triggered by factors associated with cellular damage, such as oxidative stress, and telomere shortening and expression of oncogenes [ 31 ]. The triggers activate several senescence genes, which initiate the actual induction of cellular senescence. The two senescence genes that play critical roles are TP53 and P16 INK4a , both are tumor-suppressor genes. The TP53 gene encodes for the P53 protein and is an activator of the cyclin dependent kinase (CDK) inhibitor P21, which will inhibit CDK4/6 activity. The P16 INK4a gene makes part of the CDKN2a or INK4a/ARF locus, which based on alternative splicing, encodes two protein products: P14 ARF , a regulator of P53 stability and the P16 INK4a protein, an inhibitor of CDK4/6. Thus, both P53 and P16 INK4a prohibit the activation CDK4/6, thus blocking the phosphorylation of the retinoblastoma protein (pRB). As a result, the cell cycle is arrested in the G 1 phase [ 32 , 33 ]. In Figure 2 an overview of the pathways involved in cellular senescence is shown.

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Object name is cancers-13-01400-g002.jpg

Pathways of cellular senescence. Due to cellular stressors like telomere shortening, DNA damage, oxidative stress and the expression of oncogenes, senescence genes are induced. The TP53 gene encodes for P53, which induces P21, a cyclin dependent kinase inhibitor (CDK) blocking CDK4/6. As a result, phosphorylation of the retinoblastoma protein (pRB) is hindered. Consequently, the cell cannot enter the S-phase and the cell cycle is arrested in the G1 phase. The INK4a/ARF locus encodes for P14 ARF and P16 INK4a protein. P14 ARF is a regulator of P53 activity: by binding mouse double minute 2 homolog (MDM2), degradation of p53 is avoided. Like P53, P16 INK4a represses CDK4/6 by which pRB is not phosphorylated and cell cycle progression is prohibited. Figure adapted from [ 32 ].

Senescent cells enter a state of irreversible growth arrest, yet they remain metabolically active. As a result, damaged cells (such as cells having oxidative, DNA damage, shortened telomeres, genomic instability, oncogenic mutations) are unable to proliferate in an uncontrolled manner, which is an important antitumor mechanism. A schematic overview of the antitumor activities of cellular senescence is shown in Figure 3 [ 33 ]. When a cell is damaged, several scenarios are possible. An antiproliferative response can be activated by which the cell becomes apoptotic or it can enter senescence. If this does not occur, the cell is able to continue replication and may form a lesion. At this stage again, both apoptotic and/or senescence programs can be activated. However, when this fails, the lesion is able to grow, cells may gain additional genetic and/or epigenetic aberrations and eventually a malignant tumor may be formed. Even if cellular senescence is induced, cells can potentially bypass the senescent state (e.g., by epigenetic changes, etc.) and undergo malignant transformation [ 25 , 26 , 31 , 33 ].

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Object name is cancers-13-01400-g003.jpg

Schematic overview of antitumor protection by cellular senescence. Damaged cells can become apoptotic, enter the state of senescence (antiproliferative responses) or continue to replicate (expansion). When the latter occurs, a lesion may form where cells, again, can become apoptotic or enter the state of senescence. If suitable defense mechanisms are absent or fail, the lesion can further expand and by gaining additional mutations, a cancerous lesion (tumor) may be formed. Moreover, senescent cells still can escape this state and become cancerous as well. Normal cells are indicated in green, damaged cells in yellow, cancer cells in red, senescent cells in blue, and apoptotic cells in grey. Reprinted with permission from ref. [ 33 ]. Copyright 2021 American Pharmaceutical Association.

Although cellular senescence is involved in normal development and ensures tissue homeostasis by limiting the growth of damaged cells, it can have detrimental effects as well. With aging, there is an accumulation of senescent cells resulting in tissue aging and eventually failure of organ homeostasis and function. Cellular senescence has been recognized as an important hallmark of aging [ 25 , 31 , 32 ]. This has been demonstrated by Tyner et al. [ 34 ], who performed a mice experiment evaluating P53 function. As explained above, P53 is a key tumor suppressor and an inducer of cellular senescence. The experiment compared P53 wild type, P53 knockout and P53 mutant mice. Mutant mice had a mutation in TP53 gene by which P53 was activated rather than inactivated. More than 45% of wild type mice and over 80% of knockout mice developed large tumors of various types. By contrast, mutant mice exhibited an increased tumor resistance since only 2 of 35 mice developed a localized tumor lesion [ 34 ]. However, compared to the other strains, the mutant mice showed an early onset and enhanced aging phenotype, resulting in reduced lifespan [ 34 ]. Noteworthy, telomere shortening has been acknowledged as an activator of P53 [ 35 ]. García-Cao et al. [ 36 ] studied the impact of P53 on the elimination of telomere-damaged cells and/or on telomere-driven aging. They saw that the number of telomere-damaged cells was lower in mice carrying extra copies of P53 compared to wild type mice, confirming the role of P53 in the elimination of telomere-damaged cells. Furthermore, an aging-promoting effect of increased P53 activity on telomere-driven aging could not be established [ 36 ]. Similar observations have been made for P16 INK4a : knocking out P16 INK4a in mice resulted in an increased frequency of cancer development and was associated with shorter survival compared to wild-type mice [ 37 , 38 ]. Furthermore, elephants carry extra copies of TP53 gene, by which they are more likely to generate an apoptotic response in damaged cells, which clarifies their tumor resistance [ 39 ]. These observations confirmed the important cancer protective role of P53.

Additionally, apart from cell cycle arrest, senescent cells exhibit a SASP, characterized by the secretion of numerous inflammatory mediators i.e., cytokines and chemokines such as IL-1α, IL-6, IL-8, and Interferon gamma (IFNγ), proteases like matrix metalloproteinases (MMPs), Cathepsin B and growth factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factor (IGF)-binding proteins [ 31 , 32 ]. SASP often has several positive functions in the short term but these can become detrimental in the long term, by promoting both the aging process and tumor development, as explained below [ 31 , 32 , 40 ]. Various effects of the SASP are shown in Figure 4 [ 32 ].

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Overview of the important SASP functions. SASP components induce wound healing, tissue remodeling and recruit immune cells. Protumor effects of the SASP are tumor cell invasion and/or migration, stimulation of vessel formation, induction of cell proliferation, and the development of an inflammatory environment. Different SASP factors establish autocrine and paracrine senescence. Figure adapted from [ 32 ].

When senescent cells are temporarily present in damaged tissue, the SASP ensures improved wound healing. However, in the long term, senescent cells and their SASP can affect tissue structure and function, which may contribute to the aging process e.g., by the secretion of MMPs. MMPs are also associated with tumor cell invasion and migration in many cancers. Furthermore, the SASP component VEGF can stimulate tumor growth by promoting angiogenesis and tumor cell invasion. Additionally, cell proliferation is enhanced by IL-6, IL-8 and MMPs. Senescent cells reinforce their own senescent phenotype via SASP, but SASP factors can also induce senescence in neighboring cells (e.g., IL-1α, transforming growth factor beta (TGF-β) and IL-6) [ 31 , 32 , 40 ]. Another crucial function of cytokines and chemokines included in SASP is the recruitment of immune cells; these ensure clearance of senescent cells and enhance the local immune response against a developing tumor (e.g., macrophages, natural killer (NK)-cells, T-cell, etc.) [ 31 , 32 , 40 ]. However, immunosuppressive cells are attracted as well (e.g., myeloid derived suppressor cells). Importantly, SASP also comprises the secretion of numerous inflammatory cytokines (e.g., IL-1α, IL-6, IFNγ, TGF-β), chemokines (e.g., IL-8, monocyte chemoattractant protein (MCP)) and other mediators (e.g., granulocyte/macrophage colony-stimulating factor, macrophage inflammatory proteins) [ 31 , 32 , 40 ]. It is likely that “inflammaging”, the low-grade, chronic state of inflammation observed in the aged, is partially generated by the SASP of senescent cells accumulating in the body. Chronic inflammation has several detrimental effects: it modifies the microenvironment and modifies functions of surrounding cells; it affects anabolic signaling (e.g., decrease of IGF-1 by IL-6 and tumor necrosis factor alpha (TNF-α)); it influences immune reactions. Mortality and many age-related diseases, such as cardiovascular diseases, diabetes, cancer, and even frailty, are associated with inflammation [ 4 , 31 , 32 , 40 ].

2.3. Immunosenescence

A functional immune system is highly important in the prevention of tumor growth. However, aging leads to a progressive decay of immune functions, referred to as immunosenescence. Due to immunosenescence, an effective immune response against a developing tumor may fail. Moreover, it has been considered as one of the leading causes of many other age-related diseases. A strong interconnection between immunosenescence and inflammaging exist, both appear to maintain and induce each other [ 41 , 42 ].

2.3.1. Innate Immunosenescence

Although aging mainly alters the adaptive immune system, the innate immune system is reshaped as well ( Figure 5 ) [ 7 , 16 , 41 , 42 ]. Noteworthy, the innate immune system is activated by pathogens but also by an inflammatory response. In addition, cells of the innate immune system are able to release inflammatory cytokines and chemokines, highlighting the link with inflammaging [ 41 ]. With aging, the number of neutrophils remains relatively stable. However, neutrophil function is altered, as demonstrated by reduced chemotaxis, phagocytosis, signaling, and increased susceptibility to apoptosis [ 7 , 16 , 42 ]. There are age-related shifts within the monocyte subpopulation, for instance the proinflammatory monocytes (CD16 + ) increase and the phagocytic monocytes (CD16 − ) decrease. This is accompanied by many functional changes of monocytes/macrophages e.g., reduced chemotaxis, phagocytosis, antigen presentation, and increased production of inflammatory cytokines [ 7 , 16 , 42 ]. In dendritic cells, antigen presentation and signaling are reduced, and myeloid dendritic cells produce more proinflammatory cytokines [ 7 , 42 ]. The total number of NK-cells increases with aging, and shifts in the subpopulations are seen i.e., a decrease of the immature, immunoregulatory (CD56 bright ) and an increase of the mature, cytotoxic NK-cells (CD56 dim ). As a result, response to cytokines and signaling is impaired, and the NK cells produce less cytokines and become less cytolytic [ 7 , 16 , 42 ]. The altered functions of innate immune cells with aging may have an effect on the adaptive immune system, which is activated when an antigen, mostly presented by antigen presenting cells of the innate immune system, is recognized by T- and/or B-cells [ 16 , 41 ].

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Overview of the age-related changes in the innate immune system, including neutrophils, monocytes, NK-cells, dendritic cells, and adaptive immune system with the cytotoxic CD8 + T-cells (most affected by aging), CD4 + T-helper cells, Tregs, and B-cells.

2.3.2. Adaptive Immunosenescence

The adaptive immune system is composed of T-cells, mainly mediating cellular immunity, and B-cells, which play a major role in antibody-mediated or humoral immunity [ 42 ]. With aging, shifts in both numbers and functions of adaptive immune cells occur ( Figure 5 ) [ 7 , 17 , 41 , 42 ]. In general, immunosenescence of the adaptive immune system is characterized by a decrease of naive cells and an accumulation of memory cells. These changes are most striking in the T-cell population [ 7 , 41 , 42 ], with more pronounced age-related alterations in the cytotoxic T-cells (CD8 + ) compared to the helper T-cells (CD4 + ) [ 17 ]. With aging, pluripotent hematopoietic stem cells (HSC), from which all immune cell types originate, are more likely to differentiate into myeloid than lymphoid cell lines [ 7 , 41 , 42 ]. More importantly, however, is the thymic involution after puberty, which results in a reduced production of naive T-cells and lowered T-cell receptor (TCR) diversity [ 7 , 17 , 41 , 42 ]. Moreover, the proliferative capacity diminishes and a lifelong exposure to numerous immune challenges further reduces TCR diversity and depletes the naive T-cell reserves by conversion into memory T-cells [ 7 , 17 , 41 , 42 ]. Various studies have demonstrated the alterations in the T-cell compartment by evaluating different subset markers. Aging is associated with an alteration of the CD4/CD8 ratio and expansion of the immunosuppressive regulatory T-cells (Tregs) [ 41 , 42 ]. Naive, central memory (CM), effector memory (EM) and terminally differentiated effector memory (TEMRA) cells are identified by assessing the expression of CD45RA and CC-chemokine receptor 7 (CCR7). The costimulatory receptors CD27 and CD28 are important markers of T-cell activation, and CD57 and killer lectin-like receptor G1 (KLRG1) are markers of senescence [ 17 , 42 ]. With age, Koch et al. saw a decrease in naive T-cells (CD45RA + , CCR7 + ) and an expansion of TEMRA T-cells (CD45RA + , CCR7 − ), which was more pronounced in the CD8 + as compared to the CD4 + compartment [ 17 ]. Additionally, the expression of the costimulatory receptors CD27 and CD28 declined, especially in CD8 + T cells, and cells with lower expression of CD27 and CD28 often had a higher expression of CD57 and KLRG1. Hence, with age, numbers of naive T-cells decrease while the frequency of late-stage differentiated/senescent memory T-cells increases [ 17 ]. Apart from an increase in the expression of senescence markers, aging can also be associated with an increase in the expression of markers of exhaustion, which include inhibitory immune checkpoints (e.g., programmed cell death protein 1 (PD-1), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), etc.) [ 7 ].

Although age-related changes in the B-cell population are less apparent, certain modifications could be identified as well. Like T-cells, B-cells originate from HSC, thus the age-related shift from lymphopoiesis to myelopoiesis also affects the B-cells. There is also a decrease in pre-B-cells and an increase in memory B-cells, the diversity and production of antibodies diminishes which eventually leads to altered B-cell functions [ 42 ].

2.3.3. Clinical Implications of Immunosenescence

As expected, immunosenescence can have important clinical implications. There is an increased susceptibility to infections, partly due to impaired innate immune cell functions and the decrease of naive T-cells [ 41 , 42 , 43 ]. In older adults, vaccination has been shown to be less efficient, which may be a result of the decrease in naive T-cells and to the lowered antigen presenting capability of dendritic cells [ 41 , 42 , 43 ]. Importantly, as mentioned before, inflammation associated with immunosenescence creates a protumor microenvironment, which together with the lower capacity to recognize neoantigens, altered immune function, and lower T-cell activation, may lead to a decreased antitumor response [ 7 , 41 , 42 , 43 ].

Noteworthy, immunotherapy mainly depends on a properly working immune system. Immunosenescence may have an important impact on the efficacy of cancer immunotherapy but also on its side effects [ 7 ]. As mentioned before, naive T-cell numbers decrease with age, memory T-cells numbers increase, and these memory cells are often senescent or exhausted [ 17 ]. Immune checkpoint inhibitors, used in immunotherapy, block the interaction between inhibitory receptors and their ligands resulting in reactivation of the immune cell. With age, expression of these inhibitory receptors (e.g., PD-1, CTLA-4), as well as senescence markers (e.g., CD57) increase, while costimulatory receptors (e.g., CD28) are lost. This might have an impact on reactivation of the T-cells, making it less effective in older adults [ 7 ]. However, in melanoma, Kugel et al. [ 44 ] observed a higher CD8/Treg ratio in the tumor, which corresponded with a higher response to anti-PD-1 therapy (Pembrolizumab) in older patients (>60 years) [ 44 ]. Importantly, it should be noted that in general, in contrast to what was seen in this study, aging is associated with an increase of Tregs [ 41 ]. Side effects associated with immune checkpoint inhibitors are often related to inflammation. As inflammation already increases with aging, the inflammatory toxicities might be more severe in older patients [ 8 ]. The underrepresentation of older patients with cancer in clinical studies is also an issue in the immunotherapy field. In addition, the few older patients who are included in trials are usually selected fit persons. The more frequent frail old population is very rarely well represented in clinical trials with new drugs. Little is known about the immune checkpoint immunotherapy efficacy or tolerability in the general older population and certainly in the more frail subgroup [ 10 ]. As of yet, literature shows inconsistent results when comparing younger and older patients treated with immune checkpoint inhibitors. Some studies show similar results in terms of efficacy and tolerability for old patients compared to younger patients while others show a lower efficacy in old patients and an increased risk of side effects [ 6 , 7 , 8 ]. However, none of these studies particularly focused on older (and certainly not frail) adults, thus the numbers of older patients included in these trials are often very small and the results should be interpreted with caution [ 6 , 7 , 8 ].

Apart from immune checkpoints, cancer antigens can be targeted by immunotherapy as well. There are two major classes of cancer antigens: tumor specific-antigens (TSA) and the tumor-associated antigens (TAA). TSAs originate from oncogenic mutations and are therefore exclusively found on tumor cells. These antigens have gained interest over the past years as they are highly cancer-specific and are therefore associated with a lower risk of side effects [ 7 , 45 ]. The immune system has never been exposed to these neoantigens and with the shrinkage of the naive T-cell pool associated with immunosenescence, immunotherapies targeting these antigens might be less effective in older patients. Nonetheless, immunotherapies targeting TAAs might be more effective in older patients. TAAs are self-antigens that are overexpressed on tumor cells and are a result of tissue differentiation. They are currently widely used as cancer immunotherapy targets, an example in breast cancer is Human epidermal growth factor receptor 2 (HER2) [ 7 , 45 ]. The immune response against TAAs mainly depends on memory cells that have already been exposed to these antigens. Nevertheless, although there is an increase of memory cells with age, the proliferation capacity and activation might be lower. Moreover, TAAs are less tumor specific and are associated with higher risk of side effects compared to TSAs as they are also found on normal cells throughout the whole body [ 45 ]. Additionally, other options in older patients might be anti-Treg therapy, stimulation of the innate immune system, chimeric antigen receptor T-cell therapy, NK-cell adoptive therapy, etc., however no data is available as of yet and the immunologic changes in older patients with cancer should be investigated more thoroughly [ 7 ].

Importantly, the age-related changes in the immune response could have substantial effects on the amount, composition and distribution of the tumor immune infiltrate [ 46 ]. First, aging might have an impact on the ability of immune cells to recognize and respond to a developing tumor. Secondly, the composition of the immune infiltrate might be altered, as there are numerous age-related shifts within the immune cell populations. Thirdly, the capacity of immune cell to infiltrate into the tumor may be affected, resulting in altered spatial distribution of the immune cells within the tumor. However, thus far, the effect of aging on the tumor immune infiltrate has only been poorly studied. By performing a detailed characterization of the tumor immune infiltrate in patients with cancers, important insights may be gained. Markers worthy of investigating are, for example, the stromal tumor infiltrating lymphocytes (sTILs), as they are easy to measure and are informative of immune cell abundance in the tumor. Moreover, composition of the immune infiltrate should be investigated as well by assessing the expression of different immune cell markers. In this regard the use of multiplexed immunohistochemistry will allow us to get a better understanding of the tumor associated immune infiltrate elucidating the significance of the coexpression of different markers in a specific cell and its relation with other immune cells or with tumor cells [ 47 , 48 ]. For instance, CD3 (T-cells), CD4 (helper T-cell), CD8 (cytotoxic T-cells), CD20 (B-cells), FOXP3 (Tregs), etc. Additionally, activation (CD27, CD28), ICs (PD-1, CTLA-4, lymphocyte-activation gene 3 (LAG-3), T-cell immunoglobulin, and mucin domain-containing molecule 3 (TIM-3)) senescence (CD57, KLRG-1), exhaustion (PD-1 and/or CTLA-4) markers could be included as well [ 7 ]. Furthermore, the spatial distribution of the immune cells has been shown to be a prognostic factor [ 49 ].

Thus, immunosenescence and inflammaging are significant consequences of the aging process and are probably the most important causes of many age-related diseases, including cancer. However, as of yet, the clinical relevance of immunosenescence and inflammaging is underexplored, especially in the cancer setting. In order to gain insights, our group performed an extensive immune biomarker study in patients of different ages (35–45, 55–65, ≥70 years old) with so called luminal B-like breast cancers [ 46 ]. Numerous profound age-related alterations, which could be linked to inflammation and/or immunosenescence, were observed in the blood immunological portrait and the local immune response. The plasma levels of several inflammatory mediators (IL-1α, IP-10, IL-8, MCP-1, and C-reactive protein (CRP)), immune checkpoint markers (Galectin-9, sCD25, TIM-3, and Programmed death-ligand 1 (PD-L1)), IGF-1 and circulating immune-related microRNAs (miRNAs) (miR-18a, miR-19b, miR-20, miR-155, miR-195, and miR-326) significantly changed with aging. Moreover, within peripheral blood mononuclear cell populations, several shifts were seen, and the population of naive cytotoxic T-cells showed to be most affected by aging. With increasing age, the tumor immune infiltrate changed as well. The total lymphocytic infiltration was lower in older patients, concomitant with lower abundance several immune cell populations (T-cells, cytotoxic T-cells and B-cells). The relative fractions of cell subsets in the immune infiltrate were also altered. In the old group, frailty-related changes were studied as well. Here, the most striking observations were the increase in exhausted/senescent (CD27 − CD28 − and/or CD57 + ) terminally differentiated cytotoxic T-cells in blood and an increased infiltration of FOXP3 + cells in the tumor. This data confirmed an age/frailty-related remodeling of both systemic immunity and the tumor immune response in patients with a luminal B-like breast cancer [ 46 ].

2.4. Treatment of Older Patients with Cancer

In several solid cancer types, tumor behavior differs with age. For example, older patients are more frequently diagnosed with a more aggressive ovarian cancer compared to younger patients while the opposite is true for breast cancer patients [ 11 ]. Importantly, at old age tumors are often more advanced at the time of diagnosis [ 50 ]. The highly heterogeneous global health status of older people and the fact that older cancer patients are highly underrepresented in clinical trials, makes elderly cancer care highly complex [ 10 , 50 ]. Even if older patients are included in clinical studies, results should be interpreted with caution; older patients who are included in clinical studies are often very fit and are therefore not representative for the general older population [ 10 ].

Thus, it is important to take into account a patient’s biological age rather than merely chronological age. A comprehensive geriatric assessment (CGA) could be used to assess a person’s biological age by determining the fitness/frailty status. This multidimensional and interdisciplinary tool evaluates several health domains via standardized questionnaires, such as functionality, mental health and social status, comorbidities, cognition, polypharmacy, and nutritional status. These elements could have an important impact on cancer development, prognosis, treatment effectiveness, and/or tolerability [ 11 ]. Declined functional status could be linked with increased mortality [ 11 , 51 ]. Comorbidities can, by themselves and/or by their specific treatments, increase the risk of developing a cancer. For instance, tuberculosis is associated with lung cancer development, and chronic inflammation and immunodeficiency are linked with several cancers [ 52 ] and statins correlated with a lower risk of developing breast, large bowel and prostate cancer [ 53 ]. Furthermore, comorbidities might affect treatment tolerability [ 52 ] and drugs administered to treat the comorbidities might interact with anticancer therapies [ 11 ]. Nutrition can also be linked with cancer, life expectancy and treatment tolerability [ 11 , 26 ]. A very important factor to take into account is dementia, which has an important impact on treatment decision: not only can the correct intake of medication be impaired but several anticancer therapies could also have neurotoxic effects (e.g., aromatase inhibitors blocking estrogen production) [ 54 , 55 ]. Thus, the frailty status of older patients but not age by itself, should be a determining factor to give a certain treatment or not. Several studies also demonstrated that frailer patients undergoing surgery are confronted with worse survival and might have more postoperative complications [ 56 ]. Independent of age, frailty status was associated with a worse overall survival and disease-specific survival in patients with breast cancer after tumor resection [ 57 ]. Overall survival of frailer patients with colorectal cancer who had a colectomy was also less favorable [ 58 ]. Tolerability of and survival after chemotherapy might also be affected by a patient’s frailty status [ 10 , 56 ]. Amongst many others, Hurria et al. established a correlation between frailty and the risk of toxicity during/after chemotherapy [ 59 ]. In breast cancer, frailty was associated with both increased toxicity and worse survival [ 60 ]. Conversely, limited literature is available on the effects of radiotherapy on frailer patients, although it is obvious that frailty might play a role here as well [ 56 ]. The potential impact of immunosenescence on the effectiveness of cancer immunotherapy has been described extensively in the previous section.

Ensuring healthy aging could be an important approach not only to prevent/treat cancer but also other age-related diseases [ 61 , 62 , 63 ]. Several factors could contribute to healthy aging. For example, caloric restriction resulted in an increased lifespan and a delay of age-related diseases in different animal models [ 26 , 61 ]. In humans, it also showed health benefits (e.g., reduced cardiac risk factors) [ 26 ]. The importance of the insulin signaling pathway [ 61 , 64 , 65 , 66 , 67 , 68 , 69 , 70 ], mechanistic target of rapamycin (mTOR) [ 61 , 69 ], sirtuins [ 61 , 71 ], circadian clock [ 61 , 72 ], and oxidative stress [ 61 , 73 ] in relation with longevity and/or age-related diseases have been extensively documented. As cancer and other age-related diseases are linked with inflammation, maintaining a good balance between pro- and anti-inflammatory mediators might be of great importance at higher age [ 61 ]. Furthermore, the use senolytic drugs (i.e., drugs eliminating senescent cells) for the treatment of senescence-associated cancers are gaining interest [ 61 , 62 , 63 ]. Data from clinical studies in humans are not available yet, however, studies in mice and human cells were very promising. For instance, Amor et al. studied chimeric antigen receptor (CAR) T-cells as a senolytic agent by targeting plasminogen activator receptor on senescent cells in mice. This resulted in better survival in mice with a lung adenocarcinoma and in mice with liver fibrosis, tissue homeostasis was restored [ 62 ]. In another study in mice, senescent cells were cleared via recombinant caspase 8 which was activated in senescent cells after treatment with the AP20187 drug, resulting in delayed onset of age-related disorders [ 74 ]. However, further research is mandatory and it should be kept in mind that senescent cells also have several beneficial effects, which may outweigh the benefits of being removed [ 63 ].

3. Aging Biomarkers

As the role of aging is largely underexplored in the cancer field so far, it is important to gain more extensive and in-depth insight in the aging process in the oncological setting. This could be achieved by studying various aging biomarkers that have been described in literature in the healthy population, some of which are listed below [ 64 , 75 ]. Additionally, as the immune system is highly affected by aging and as it is an important factor in cancer development but also in cancer immunotherapy, markers of immunosenescence are also highly relevant in a cancer context. Moreover, a better understanding of the impact of aging on tumor immunity is mandatory, especially in view of increasing clinical successes of cancer immunotherapy. Here below, we summarize some of the most studied and relevant aging biomarkers in the general older population that could be relevant for future research in cancer patients.

3.1. Gene Expression

Age-related changes of gene expression contribute to the physiological alterations observed with human aging and could thus be studied as well [ 12 , 64 ]. Vo et al. compared the abundance of a selection of 148 transcripts involved in immunosenescence and stress response in PBMC from healthy young, middle aged and old persons and found 16 differentially abundant transcripts that can be considered as easily accessible biomarkers of aging [ 21 ]. Some of these age-related genes are involved in T-cell function (e.g., CD28, CD69, lymphocyte protein tyrosine kinase ( LCK ): decreased abundance in old subjects), in inflammatory reactions and in oxidative stress response (e.g., tumor necrosis factor receptor superfamily member 1A ( TNFRSF1A ), heme oxygenase 1 ( HMOX1 ) and heat shock protein family A member 6 ( HSPA6 ): increased abundance in old subjects). This is in agreement with the T-cell hypo-responsiveness and the low-grade proinflammatory status observed in old persons and could thus contribute to the lack of appropriate (tumor) immune responses in older compared to younger persons [ 21 ]. Peters et al. identified 1497 genes in whole blood with a differential expression with chronological age. Moreover, they were able to identify several cluster of genes, which could be linked to different age-related alterations e.g., immunosenescence, altered RNA metabolism functions, etc. [ 76 ]. Several other genes have been linked to the aging process, such as low density lipoprotein receptor-related protein 1B ( LRP1B ), paraoxonase 1 ( PON1 ), ‘ataxia telangiectasia mutated’ ( ATM ) gene, p21/CDKN1A gene, p53 protein, insulin/IGF-1 signaling (IIS) components, telomerase RNA component ( TERC ), IL-1 gene, IL-6 gene , Toll-like receptors genes ( TLR ) [ 77 ].

3.2. Single Nucleotide Polymorphism

Genetic predisposition plays a determining role in healthy longevity vs. frailty development. A single nucleotide polymorphism (SNP) is a DNA sequence variation at a single nucleotide position. With regard to aging, a specific SNP within the forkhead box O3 (FOXO3a) gene has been associated with longevity and SNPs in apolipoprotein E (APOE) have been correlated with an age-associated phenotype [ 78 , 79 ].

3.3. DNA Methylation Profiles

Altered DNA methylation also appears to be associated with the aging process [ 64 , 80 ]. These altered DNA methylation patterns are caused by numerous extrinsic factors e.g., lifestyle, environmental factors. DNA methylation mostly alters cytosine nucleotides followed by a guanine nucleotide, called CpG dinucleotides [ 81 ]. CpG methylation of the genome ensures genomic stability and it acts as a repressor of DNA recombination at telomeres [ 81 , 82 ]. Additionally, methylation of CpG sites in the promoter of a gene may inhibit gene expression, making DNA methylation an important player in gene regulation and “silencing”. Interestingly, age-related hypomethylation of the global genome is well-documented, while, on the other hand, many specific CpG sites are subject to age-related DNA hypermethylation. Several age-dependent CpG signatures have recently been reported as “DNA methylation age” biomarkers that can predict all-cause mortality [ 83 ]. Weidner et al. showed that assessing DNA methylation at three age-related CpG sites could predict age [ 80 ].

3.4. Telomere Attrition

Telomeres are complex, repetitive regions consisting out of (TTAGGG) repeats and associated proteins. With each cell division, and thus with increasing age, telomeres that ensure genomic integrity by protecting the end of DNA chromatids are shortened, and when becoming critically short they can induce cellular senescence [ 25 ]. Leukocyte telomere length has been suggested as a biomarker of biological aging [ 12 , 64 ]. In a study of Cawthon et al. shorter telomere length was associated with worse survival due to higher rates of heart and infectious diseases [ 22 ]. Furthermore, Mons et al. demonstrated that telomere length was associated with age and all-cause mortality [ 84 ].

3.5. Oxidative Stress Markers

One of the mechanistic explanations of the aging process is the oxidative stress/free radical theory. Due to metabolic processes and mitochondrial respiration, reactive oxygen species are produced, which exist in the cell in equilibrium with antioxidant molecules [ 28 , 29 ]. Oxidative stress increases with age, leading to accumulation of oxidation products of lipids (e.g., isoprostanes), nucleic acids (e.g., RNA derived 8-hydroxyguanosine or DNA derived 8-hydroxy-2′-deoxyguanosine) and proteins (e.g., nitrotyrosine), that exert deleterious effects and ultimately cause cellular dysfunction [ 64 ]. Isoprostanes, 8-hydroxyguanosine and 8-hydroxy-2′-deoxyguanosine can be measured as aging biomarkers in plasma [ 85 ]. Simonek et al. reported an increase of 8-hydroxy-2′-deoxyguanosine with aging [ 86 ], and in a study of Montine et al. the level of isoprostanes increased with aging [ 87 ].

3.6. Plasma miRNA Profiles

miRNAs are small noncoding RNAs which are 21–25 nucleotides in length. They mediate post-transcriptional gene silencing through either translational repression or targeting of the messenger RNA for degradation. They play a critical role in numerous physiological pathways, developmental processes and pathological conditions [ 64 ]. Dysregulation of specific miRNAs is associated with several disorders (e.g., cancer, cardiovascular diseases, etc.). It is believed that miRNAs also play a role in aging, immunosenescence and inflammation but also frailty [ 64 , 88 , 89 , 90 , 91 , 92 ]. By consequence, miRNA signatures could also be interesting as potential aging/immunosenescence/inflammation markers, especially since plasma miRNAs have recently been recognized as sensitive, specific and extremely stable biomarkers [ 64 , 88 , 89 ]. For instance, miR-20a and miR-181a have been reported as aging associated plasma miRNAs [ 64 , 88 ]. The miR-17–92 cluster and miR-155 are highly involved in immunological processes [ 89 , 90 ] and important inflammatory miRNAs are miR-155 and miR-21 [ 64 , 91 ]. Additionally, the expression levels of particular miRNAs seem to correlate with clinical frailty, e.g., miR-92a and miR-326 [ 92 ]. In our own biomarker study six immune-related plasma miRNAs showed different expression levels between different age groups. These included three members of the miR-17–92 cluster namely miR-18a, miR-19b and miR-20a. miR-18a decreased with age whereas miR-19b and miR-20a peaked in the middle-aged group but had the lowest expression in the oldest age group. The latter was also true for miR-195, which is associated with T-cell activation. Noteworthy, the miR-326 could only be measured in the oldest age group [ 46 ].

3.7. Proteostasis

Aging as well as several age-related diseases (including cancer) are associated with loss of proteostasis due to impairment of chaperoning, proteasome activity and autophagy–lysome activity [ 25 , 26 ]. However, these systems are rather activated in a cancer context [ 26 ], making interpretation of changes in these markers very difficult in older patients with cancer.

3.8. Markers of Inflammation

Aging has been associated with a low-grade, chronic state of inflammation, also referred to as inflammaging. Apart from the above-mentioned miRNAs, inflammation can be assessed by measuring plasma levels of numerous inflammatory mediators. Several reports have described a gradual increase in circulating proinflammatory cytokines (e.g., IL-1, IL-6, TNF-α), chemokines (e.g., IL-8, MCP-1) and other inflammation markers (e.g., CRP), concomitant with a decrease in anti-inflammatory mediators (e.g., IL-10) with increasing age. Circulating levels of inflammatory mediators are often elevated prior to cognitive decline, dementia and loss of physical performance [ 75 , 93 , 94 ]. At the cellular level, these markers of inflammation are also associated with cellular senescence, more particular with the SASP. In our cancer cohort, a clear increase of several inflammatory mediators was observed. With aging higher plasma levels of inflammatory cytokines (IL-1α), chemokines (IP-10, IL-8, MCP-1) and the clinical inflammation biomarker CRP were seen [ 46 ].

3.9. T-Cell P16 INK4a Expression

In our previous biomarker study, an increase of T-cell P16 INK4a expression with increasing age was noted in patients with luminal B-like breast cancer [ 46 ]. Cellular senescence is one of the most important hallmarks of aging [ 25 ]. The expression of the senescence marker P16 INK4a in T-cells has been described as a biomarker of lymphocyte senescence and thus aging of the immune system. In healthy humans, P16 INK4a expression increases markedly in peripheral blood T-cells with physical inactivity and exposure to mutagens such as tobacco. In addition, the expression of P16 INK4a increases with chronological age, with an average 10-fold increase between the ages of 20 and 80 [ 19 ].

3.10. Shifts in Immune Cell Subpopulations

As already pointed out above, numerous age-related changes occur in the cellular components of the innate and even more pronounced in the adaptive immune system [ 16 , 17 ]. These changes can be demonstrated by flow cytometric subtyping of the different immune cell populations [ 17 ]. Interesting markers to include in such analysis are CD14 and CD16 to distinguish different monocyte subpopulations, and CD56 and CD16 to identify different NK subpopulations [ 16 ]. CD4 and CD8 can identify the helper T-cells and cytotoxic T-cells of the adaptive immune system. A distinction between naive and memory cells can be made with the help of CD45RA and CCR7 expression. Moreover, activation status can be assessed by evaluating CD27 and CD28 whereas CD57 is a marker of senescence [ 17 ]. Koch et al. analyzed CD4 and CD8 T-cell subsets via flow cytometry and observed a decrease of naive cells and an increase of late-differentiated T-cells, especially those expressing CD8 [ 17 ]. Sadeghi et al. showed higher levels of inflammatory monocytes (CD14 dim CD16 bright ) with age [ 95 ] and Chidrawar et al. demonstrated that CD56bright NK-cell abundance decreased with increasing age [ 96 ]. In our breast cancer cohort, we observed an increase of intermediate monocytes with age. However, most notable were the effects of age on the naive CD8 population. Within the CD8 population we also saw a loss of CD27 and/or CD28 [ 46 ].

3.11. Markers of Cellular Senescence

At the cellular level, the SASP as well as elevated P16, P53 and P21 levels are described as important markers of cellular senescence. Additionally, increased levels of the DNA damage marker γ-H2AX, higher degree of β-galactosidase activity and the formation of high levels of senescence-associated heterochromatin foci characterize senescent cells [ 25 , 64 , 97 ].

3.12. Circadian Clock

With age, the circadian rhythms change, which has an important impact on several biological processes. For example, older adults’ sleeping patterns are different, which may increase the risk of cognitive decline [ 72 , 98 ]. Melatonin levels decrease with aging and may be associated with age-associated cognitive disorders [ 72 ]. Numerous metabolic process are regulated by circadian clocks such as glucose homeostasis, lipid metabolism, as well as inflammation [ 72 ]. Moreover, a connection between deregulation of the circadian clock and cancer has been described [ 99 , 100 ]. Several studies showed that sleep disruption increased the risk of developing e.g., breast [ 101 ] and prostate cancer [ 102 ]. Conversely, optimizing circadian rhythms might improve outcome, e.g., cortisol levels were associated with lung cancer survival [ 103 ].

3.13. IGF-1

One of the hallmarks of aging is dysregulated nutrient sensing with an important role for the insulin/IGF-1 signaling pathway [ 64 ]. IGF-1 can activate the insulin receptor but also has important growth stimulating effects. The plasma levels of circulating IGF-1 have been shown to decrease with aging. This was also confirmed in our cancer cohort [ 46 ]. Diminished IGF-1 signaling has been associated with longevity in several mouse studies [ 65 , 66 ], some studies in humans could confirm this, however, results are often inconsistent [ 65 , 66 , 67 , 68 ]. Noteworthy, reduced IGF-1 signaling has been linked to an improved functional status [ 67 ]. Studies in mice but also some studies in older humans showed that diminished IGF-1 signaling has been associated with an improved functional status. Moreover, although the link between IGF-1 levels and age-related diseases is not fully established, it has been demonstrated that increased levels of IGF-1 are associated with tumor development, whereas it might reduce the risk of cognitive decline, dementia and cardiovascular disease [ 67 , 69 , 70 ].

3.14. Microbiome

The gut microbiome might be an important factor in healthy aging as it has been acknowledged as an important regulator of metabolic processes, immunity and inflammation [ 25 , 104 ]. With aging the microbiota composition becomes less diverse and there are changes in the abundance of specific species [ 104 ]. Analyzing the gut microbiome might give important information; for example, Biagi et al. showed that extreme longevity was associated with an increased abundance of Christensenellaceae, Akkermansia and Bifidobacterium [ 105 ]. Moreover, frailty seems to be associated with a reduced microbiota diversity [ 106 ]. Studies in mice already showed that modulation of the microbiome might delay immunosenescence. In humans Shen et al. demonstrated that decreased levels of Bacteriodetes might be linked to immunosenescence [ 107 ]. Additionally, the microbiome association between cancer development and anticancer therapies have been made [ 108 ]. Helicobacter pylori is a widely acknowledged oncogenic organism [ 109 ] and several studies show a relation between treatment response and the gut microbiome [ 108 ].

3.15. Biomarker Panels

Recently, we evaluated blood immunosenescence signatures potentially reflecting age or frailty. This was done by assessing individual biomarkers as well as 3-biomarker panels and their ability to divide patients into the correct age/frailty group. This study revealed that blood biomarker panels performed better than individual biomarkers, and that these panels did not only accurately reflect a patient’s chronological age, but more importantly the patient’s frailty status (manuscript submitted). These findings confirmed the potential utility of biomarkers in geriatric oncology.

4. Conclusions

The link between aging and cancer has been widely acknowledged, a schematic overview can be seen in Figure 6 . The lifelong exposure to numerous endogenous as well as exogenous factors, the chronic state of inflammation and immunosenescence contribute to an increased risk of developing cancer with advancing age. However, the biological age of each individual is unique and is not reflected by their chronological age but rather by frailty status. Here we described several potential aging biomarkers that may provide more in depth view of the aging/frailty status as compared to clinical interpretation only, the implementation of aging biomarkers or a combination of them in clinical practice could aid with the determination of a person’s true age and therefore with (oncological) decision-making. Moreover, as aging has important effects on several biological process, the effectiveness and tolerability of certain treatments (e.g., cancer immunotherapy) could be altered in older patients. Thus, selecting the most suitable treatment for older patients is highly important yet extremely difficult. This warrants further and more extensive investigation in these older patients. Better clinical insight of older patients and the identification of robust, reliable biomarkers could aid with a better individualized treatment for older patients with cancer.

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Schematic overview of strong interconnection between aging and cancer. The discussed biomarkers of aging are summarized as well as the clinical symptoms of frailty. The aging process and cancer share several biological processes impacting oncological decision making. However, treatment choices, toxicity and tolerability and treatment efficacy are highly influenced by age and more importantly frailty status. Taking all this together, age and frailty have an immense impact on the risk of developing cancer, cancer biology, prognosis, and therapy choices and thus the outcome for older patients with cancer.

This research received no external funding. HW is a recipient of the “Fonds voor Wetenschappelijk Onderzoek–Vlaanderen (FWO).” GF is recipient of a post-doctoral mandate from the Klinsche Onderzoek en OpleidingsRaad (KOOR) of the University Hospitals Leuven.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Conflicts of interest.

The authors declare no conflict of interest.

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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1. Essay on Cancer Treatment: (Around 200 Words) Success of Cancer Treatments: The success rates for current cancer treatments are strongly influenced by the stage at which the disease is diagnosed. When cancer is detected early and tumor cells are still localized to their initial site of origin, cure rates tend to be very high, even for ...
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What Is Cancer?

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Cancer and Aging: Two Tightly Interconnected Biological Processes

Giuseppe Floris

Hans Wildiers

Sigrid Hatse

1. Introduction

2. Mechanistic Interface between Aging and Cancer

2.1. Cellular Damage and DNA Damage Response

2.2. Cellular Senescence

2.3. Immunosenescence

2.3.1. Innate Immunosenescence

2.3.2. Adaptive Immunosenescence

2.3.3. Clinical Implications of Immunosenescence

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