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Cancer Survivors: In Their Words

This year alone, an estimated 1.8 million people will hear their doctor say they have cancer. The individual impact of each person can be clouded in the vast statistics. In honor of National Cancer Survivor Month,  Cancer Today would like to highlight several personal essays we’ve published from cancer survivors at different stages of their treatment. 

In  this essay , psychiatrist Adam P. Stern’s cerebral processing of his metastatic kidney cancer diagnosis gives rise to piercing questions. When he drops off his 3-year-old son to daycare, he ponders a simple exchange: his son’s request for a routine morning hug before he turns to leave. “Will he remember me, only a little, just enough to mythologize me as a giant who used to carry him up the stairs? As my health declines, will he have to learn to adjust to a dad who used to be like all the other dads but then wasn’t?” he questions. 

In  another essay from a parent with a young child, Amanda Rose Ferraro describes the abrupt change from healthy to not healthy after being diagnosed with acute myeloid leukemia in May 2017. After a 33-day hospital stay, followed by weeklong chemotherapy treatments, Ferraro’s cancer went into remission, but a recurrence required more chemotherapy and a stem cell transplant. Ferraro describes harrowing guilt over being separated from her 3-year-old son, who at one point wanted nothing to do with her. “Giving up control is hard, but not living up to what I thought a mother should be was harder. I had to put myself first, and it was the hardest thing I had ever done,” she writes.

In January 1995, 37-year-old Melvin Mann was diagnosed with chronic myelogenous leukemia, which would eventually mean he would  need to take a chance on a phase I clinical trial that tested an experimental drug called imatinib—a treatment that would go on to receive U.S. Food and Drug Administration approval under the brand name Gleevec. It would also mean trusting a system with a documented history of negligence and abuse of Black people like him: “Many patients, especially some African Americans, are afraid they will be taken advantage of because of past unethical experiments like the infamous Tuskegee syphilis study​,” Mann writes, before describing changes that make current trials safer. Mann’s been on imatinib ever since and has enjoyed watching his daughter become a physician and celebrating 35 years of marriage.

In  another essay , Carly Flumer addresses the absurdity of hearing doctors reassure her that she had a good cancer after she was diagnosed with stage I papillary thyroid cancer in 2017. “What I did hear repeatedly from various physicians was that I had the ‘good cancer,’ and that ‘if you were to have a cancer, thyroid would be the one to get,’” she writes.

In another piece for Cancer Today , Flumer shares  how being diagnosed with cancer just four months after starting a graduate program shaped her education and future career path.

For Liza Bernstein, her breast cancer diagnosis created a paradox as she both acknowledged and denied the disease the opportunity to define who she was. “In the privacy of my own mind, I refused to accept that cancer was part of my identity, even though it was affecting it as surely as erosion transforms the landscape,” she writes . “Out in the world, I’d blurt out, ‘I have cancer,’ because I took questions from acquaintances like ‘How are you, what’s new?’ literally. Answering casual questions with the unvarnished truth wasn’t claiming cancer as my identity. It was an attempt to dismiss the magnitude of it, like saying ‘I have a cold.’” By her third primary breast cancer diagnosis, Bernstein reassesses and moves closer to acceptance as she discovers her role as advocate.

As part of the staff of  Cancer Today , a magazine and online resource for cancer patients, survivors and caregivers, we often refer to a succinct tagline to sum up our mission: “Practical knowledge. Real hope.” Part of providing information is also listening closely to cancer survivors’ experiences. As we celebrate National Cancer Survivor Month, we elevate these voices, and all patients and survivors in their journeys.

Cancer Today is a magazine and online resource for cancer patients, survivors, and caregivers published by the American Association for Cancer Research.  Subscriptions to the magazine are free ​ to cancer patients, survivors and caregivers who live in the U.S. 

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The Unique Hell of Getting Cancer as a Young Adult

W hen I got diagnosed with Stage 3b Hodgkin Lymphoma at age 32, it was almost impossible to process. Without a family history or lifestyle risk factors that put cancer on my radar, I stared at the emergency room doctor in utter disbelief when he said the CT scan of my swollen lymph node showed what appeared to be cancer—and lots of it. A few days away from a bucket list trip to Japan, I’d only gone to the emergency room because the antibiotics CityMD prescribed to me when I was sick weren’t working.I didn’t want to be sick in a foreign country. So when the doctor told me of my diagnosis, the  only question I could conjure was: “So Tokyo is a no-go?”

Around the world, cancer rates in people under 50 are surging, with a recent study in BMJ Oncology showing that new cases for young adults have risen 79% overall over the past three decades. In the U.S. alone, new cancer diagnoses in people under 50 hit 3.26 million, with the most common types being breast, windpipe, lung, bowel, and stomach. A new feature in the Wall Street Journal highlights the mad dash among doctors and researchers to determine what’s causing this troubling rise. Strangely, overall cancer rates in the U.S. have dropped over the past three decades, while young people—particularly with colorectal cancers—are increasingly diagnosed at late stages. “We need to make it easier for adolescents and young adults to participate in clinical trials to improve outcomes and study the factors contributing to earlier onset cancers so we can develop new cures,” says Julia Glade Bender, MD, co-lead of the Stuart Center for Adolescent and Young Adult (AYA) Cancers at Memorial Sloan Kettering in New York City (where I am currently a patient.)

Doctors suspect that lifestyle factors and environmental elements, from microplastics to ultra-processed foods, could be to blame. But many adults in their 20s and 30s, such as myself, were otherwise healthy before their diagnoses. It felt like all those years of forcing myself to run, eat high-fiber foods, and choke down kombucha were for nothing. 

Cancer is hell at any age, but the challenges facing young adults are especially steep, as the disease disrupts a formative period for building a career, family, and even healthy self-esteem, from body image to gender identity. It’s critical that our approach to treating and supporting these patients reflects the severity of this disruption. In recent years, a growing number of cancer hospitals have developed young adult-specific programming like support groups, information sessions on dating and sexual health, and even mobile apps to help counter social alienation. But there is still a long way to go.

Read more: Why I Stopped Being A “Good” Cancer Patient

Shockingly enough, canceling my trip to Japan was the least of my worries. Beyond the excruciating physical side effects of high-dose chemotherapy and a number of life-threatening complications, cancer pulverized my self-esteem into nothingness, as I watched peers get married and promoted from my bed. Thankfully, after switching to a new hospital, I found support groups that connected me with a community of peers who got it, as well as social workers who work exclusively with young adults and thus recognized many of my biggest challenges, like social isolation, financial strain, the dating nightmare, and hating my bald head.

Perhaps the biggest reason I resented cancer was for disrupting a milestone I’d worked for my whole life: a book launch. (My diagnosis came two months before my first book was published.) Young adulthood is meant to be littered with these kinds of professional and personal benchmarks, many of which are hard enough to accomplish without tumors; dating, for instance, is impossible for me even as a healthy person. Now I have to re-enter the pool older, weaker, and more traumatized? 

“Young adult patients may be trying to assert independence from parents, establish a career or intimate relationship, or even be parents themselves,” says Bender. “Most will be naïve to the medical system or a serious health condition.” And so they require flexible, creative clinicians who can help navigate them “to and through the best available therapy and back to their lives, inevitably ‘changed’ but intact.” Not only do these patients need specialized psychosocial support, but research initiatives should prioritize developing treatments that minimize long-term toxicities.

Given that many young patients haven’t yet built financial stability and are often in some form of debt, organizations like Young Adults Survivors United (YASU) have emerged to support young adult survivors and patients through the financial overwhelm. Stephanie Samolovitch, MSW and founder of YASU, says that there’s still an enormous need for resources supporting young adult cancer patients and survivors.

“Cancer causes a young adult to be dependent again, whether it’s moving back in with parents, getting rides to appointments, or asking for financial help,” says Samolovitch, who was diagnosed with leukemia in 2005, two weeks before her 20th birthday. “Young adults never expect to apply for Medicaid or Social Security Disability during our twenties or thirties, yet cancer doesn't give us a choice sometimes. That causes stress, shame, depression, and anxiety when trying to navigate the healthcare system.”

Read more: How to Create an Action Plan After a Cancer Diagnosis

When Ana Calderone, a 33-year-old magazine editor, was diagnosed with stage 2 breast cancer at 30, the most challenging part of getting diagnosed so young was “everything.”

“I felt like it set my whole life back, which sounds stupid because I was literally fighting for my life,” she says. “Who cares if I had to delay my wedding a year because I was still getting radiation treatment? But it was really hard at the time. Everything was delayed, and still is.”

During chemo, Calderone’s doctors gave her a shot that she still receives to try and preserve her ovaries, and she’s been able to try IVF twice. She says she had to proactively advocate for those things with her care team. While Calderone is currently cancer free, she still must take medication that has further delayed her plans to build a family. “I’m fairly confident I’d have a child by now if I didn’t get cancer. That’s been the most devastating part,” she says. “My oncologist would consider letting me get pregnant in two more years, which would be 4.5 years post-diagnosis, and even that is still a risk.”

For 32-year-old Megan Koehler, whose son was one and a half when she was diagnosed with Hodgkin Lymphoma, the hardest part “was knowing the world continued on while I spent days in bed,” she says. “My coworkers still worked on projects I was supposed to be part of, and the worst was knowing my son was growing up, learning to speak sentences, and just becoming a toddler without me – or so it felt that way.” 

She remembers crying for most of his second birthday because she was in bed post chemo, feeling devastated that she didn’t have the energy to spend the day with him. During a 50-plus day hospital stay caused by an adverse reaction to a chemotherapy drug, she would Facetime him and cry when he spoke in sentences, because he wasn’t doing that before she was admitted. While she’s grateful for the support she had from her husband and mother, she felt alienated. “I spoke to a few people my age via social media, but no one in person. My center mostly catered to the older generations, so it was somewhat isolating. I did have a great relationship with a few of the infusion nurses who were around my age.”

While oncologists may be rightly focused on saving patients’ lives, there must be more consideration for quality of life during and after treatment – both physical and mental. “More questions need to be asked about their relationships, fertility options, and any mental health concerns or symptoms,” says Samolovitch. From a research perspective, initiatives must expand to pinpoint not only the reason for the rise of cancer in young adults, but find ways to screen and diagnose earlier.

Towards the beginning of my treatment, before I switched hospitals, my oncologist seemed to treat my concerns about self-esteem and hair loss as trivial compared to the real work of saving my life. At my weakest, I had to advocate repeatedly to get accurate information on cold capping, a process of scalp cooling that can preserve most of your hair during chemotherapy, and I had to beg again and again for a social worker to reach out to me, which took weeks. 

It’s a beautiful thing that more young adults with cancer are surviving their illnesses. But that means they’ll have decades of life ahead of them. Providers must do a better job supporting young adult patients through all the collateral damage that comes with cancer and its treatment.  

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Essays on blood: why do we actually have it?

Adjunct Professor, University of Technology Sydney

Disclosure statement

David Irving is employed by the Australian Red Cross Blood Service and has research collaborations with others receiving NHMRC and ARC research grants. Australian governments fund the Australian Red Cross Blood Service for the provision of blood, blood products and services to the Australian community.

University of Technology Sydney provides funding as a founding partner of The Conversation AU.

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This week we’re running a series in collaboration with the Australian Red Cross Blood Service looking at blood: what it actually does, why we need it, and what happens when something goes wrong with the fluid that gives us life. Read other articles in the series here .

Just as a village can’t grow into a city without some form of transport (road, rail or river) that provides necessary interconnections for it to flourish, living things are limited in the size they can reach unless they have some form of circulatory system to transport nutrients and remove waste.

Single celled organisms such as bacteria and fungi, and some multicellular creatures such as sponges, corals and flatworms, simply absorb the nutrients they need and get rid of their waste using a passive process known as diffusion (which is much like soaking in and draining out).

More complex animals have developed some kind of circulatory system. A variety of different systems and pumps (hearts) have developed, but they all have a few things in common. These include something to carry oxygen around their bodies, a fluid of some sort, and some “plumbing” – in humans (and a number of other species) the fluid is called blood and the plumbing is our arteries, veins and capillaries. The oxygen carrier is haemoglobin.

Depending on the organism and where it has adapted to live, its oxygen carrier can come in different forms, often giving its “blood” different colours. Spiders, crustaceans, octopuses and squid use haemocyanin, which is based on copper and gives them blue blood. This carrier works well in low oxygen environments and in the cold.

Segmented worms and some leeches use an iron based carrier called chlorocruorin, which can appear either green or red, depending on its chemical environment. Vertebrates, including humans, use haemoglobin, which makes their blood red.

A truly special case is the Antarctic icefish , which lost its haemoglobin long ago as a result of a presumably random mutation. It has adapted though, and now survives by transporting oxygen that is simply dissolved in its blood. This is possible thanks to the cold conditions it lives in.

What is our blood made of?

Human blood, and that of all creatures with backbones (Antarctic ice fish excepted), is red. The colour comes from a chemical known as haem, which contains iron. It’s the iron that is the crucial ingredient for carrying oxygen. Oxygen is needed for our cells to burn sugars, fats and proteins in a controlled way. This provides us with the energy we need to live.

Outside our bodies, we know that when iron is exposed to oxygen, it rusts. And it doesn’t easily “unrust”. But to work as an oxygen carrier in our bodies, iron needs to “rust” and “unrust” on demand - picking up oxygen where it is in plentiful supply (our lungs), and releasing it where it is required (the cells in our organs).

This on/off oxygen switch is made possible with help from complex larger molecules. The first is haem, a flat ring structure that holds an iron atom at its centre. Haem is held closely by proteins known as globin, and this combination forms haemoglobin, which is itself packaged up in red blood cells to be transported around the body.

Infographic - From animal experiments to saving lives: a history of blood transfusions

The molecular structure of haemoglobin is delicately tuned to allow it to bind oxygen in the lungs and drop it off in areas where there is less oxygen available.

Red cells are specialised parcels, lacking DNA, that are able to squeeze through the tiniest capillaries, down to four millionths of a meter (equivalent to roughly half their diameter). Their donut shape maximises their surface area to make sure they can efficiently deliver oxygen, while keeping them small enough to fit through the smallest blood vessels.

More than just the red stuff

As well as red cells, our blood contains other cells and chemicals that repair and maintain the transport system and send signals around the body.

White blood cells, also known as leukocytes, repel or destroy invaders. Some white blood cells (lymphocytes) manufacture molecules known as antibodies that tag viruses and bacteria for destruction, while others called neutrophils and macrophages (literally “big eaters”) engulf bacteria, fungi and parasites to keep our circulation clean. When neutrophils have done their job you sometimes might see them as the main component of pus.

Platelets are very small fragments of larger cells called megakaryocytes. They react to any breaches to the walls of blood vessels, gathering together and triggering reactions that form a plug (or a clot) for the damaged section. If a person doesn’t have enough platelets, they can suffer from uncontrollable bleeding.

Where does it come from?

All blood cells (red cells, white cells and platelets) develop from haematopoietic (literally meaning “blood-making”) stem cells, located in the bone marrow. It has recently been found that many platelets are made in the lungs , from megakaryocytes that have migrated there from the bone marrow.

As stem cells develop, they progressively specialise into the many different types of blood cells, making developmental choices along the way. The specialisation of cells during development is tightly controlled by a symphony of growth factors. In some types of blood cancers and serious diseases, stem cell or bone marrow transplants can be used to “reboot” the blood making system.

As our knowledge of the control of blood cell development grows, we’re making progress towards being able to reproduce this process in cells grown in the laboratory . This is still some time away from being a broadly available process, but an exciting area to watch as it develops.

Update: the sentence outlining the shape of red blood cells was incorrect and has been reworded.

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What Is Cancer?

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A dividing breast cancer cell.

The Definition of Cancer

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

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

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

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

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

Differences between Cancer Cells and Normal Cells

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

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

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

How Does Cancer Develop?

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

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

Genetic changes that cause cancer can happen because:

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

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

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

Fundamentals of Cancer

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

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

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

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

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

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

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

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

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

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

Types of Genes that Cause Cancer

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

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

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

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

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

When Cancer Spreads

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

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

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

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

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

Tissue Changes that Are Not Cancer

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

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

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

Types of Cancer

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

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

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

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

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

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

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

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

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

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

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

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

Our page on soft tissue sarcoma has more information.

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

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

Our page on leukemia has more information.

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

There are two main types of lymphoma:

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

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

Our page on lymphoma has more information.

Multiple Myeloma

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

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

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

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

Brain and Spinal Cord Tumors

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

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

Other Types of Tumors

Germ cell tumors.

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

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

Neuroendocrine Tumors

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

Our definition of neuroendocrine tumors has more information.

Carcinoid Tumors

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

Our page on gastrointestinal neuroendocrine tumors has more information.

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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.

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Essay on Cancer for Students and Children

500+ words essay on cancer.

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

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

Types of Cancers

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

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

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Causes of Cancer

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

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

Treatment of Cancer

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

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

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3 Things to Understand About Rare, Chronic Blood Cancers, According to a Patient

When it comes to her outlook on life, Donna* always sees her glass as half full. She's such an optimist, in fact, that you might not guess upon first meeting her that in her mid-sixties, she's living with a rare, chronic blood cancer.

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Her journey began in 2011, when she started to feel symptoms — such as chronic hypertension, fatigue and dizziness — that were mistaken for other health problems. As a speech-language pathologist (or speech therapist) and motivational speaker, Donna travels frequently across the country as a speaker for educators. Her symptoms became so debilitating that she struggled to walk the hundred yards to her mailbox. "I used to get halfway and have to sit down in the middle of the road and start crying," she says. Despite many visits to her doctor, she never received a clear explanation for her symptoms until she was referred to an oncologist who ultimately diagnosed her with polycythemia vera. From that point on, she began her journey in understanding how to live with a rare cancer and how to manage this diagnosis.

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Polycythemia vera, or PV, is part of a group of rare, chronic blood cancers known as myeloproliferative neoplasms, or MPNs. They develop when the body's bone marrow does not work properly, causing it to produce too few or too many red or white blood cells or platelets depending on the form of MPN, according to the MPN Research Foundation .

MPNs can affect people at any age, but are more common in people over 50. There is no cure, but people with MPNs can generally live for a long time with proper treatment. More than 200,000 people in the United States are estimated to be living with an MPN, according to the Leukemia & Lymphoma Society .

Beyond the numbers and the science, there are three key things Donna wants people to know about her experience of living with an MPN like PV.

1. Speak Up About How You're Feeling

Donna had been sick with various symptoms that were attributed to other conditions for years before she went to her nurse practitioner and said, "You know, someone's missing something," she says. She felt that she was dealing with something more pervasive, so she requested additional lab work.

Upon further review of her blood work, Donna's nurse referred her to a hematologist oncologist — a doctor who specializes in treating blood cancer — who in turn referred her to an MPN specialist. After a bone marrow biopsy, the specialist was able to provide the answers Donna was looking for: She had been living with PV.

Her oncologist prescribed a type of oral chemotherapy called hydroxyurea (HU). "Even though I tried to keep an open mind, my body would not tolerate it, and within a week of taking it I felt worse," Donna says.

After three months of her bloodwork being within healthy levels, but side effects from the HU like fatigue and body aches persisting and worsening, she told her doctor that she could not bear the side effects on a daily basis. That's when stopped receiving HU treatment and was prescribed a medication called Jakafi ® (ruxolitinib), a prescription medicine used to treat adults with PV who have already taken hydroxyurea and it did not work well enough or they could not tolerate it.

"In PV, control of the hematocrit — volume of blood taken up by red blood cells — is thought to be very important," Peg Squier, MD, PhD, and group vice president for U.S. medical affairs at Incyte, the makers of Jakafi, says. "In clinical trials, Jakafi was shown to help control patients' hematocrit without requiring phlebotomy — the common treatment practice of taking blood out of the veins to decrease blood volume. Jakafi also helped reduce enlarged spleen in these patients — a commonly experienced symptom amongst patients with PV."

"Physical exhaustion, mental fatigue, itching, abdominal discomfort, night sweats and bone or muscle pain can all be symptoms of PV," Squier says. "These common symptoms can easily be attributed to something else, such as menopause or aging, which can result in PV going undetected by health care providers. This is why it's so important for people living with PV who experience new or changing symptoms to proactively bring them up to their health care teams."

Though her symptoms can sometimes greatly affect her daily life, Donna works closely with her health care team to manage her condition. She credits that to learning more about the disease — which she had never heard of before her diagnosis — and finding the right treatment for her.

"I am proud that I had the courage to tell my doctor my initial treatment just wasn't working for me," she says. "I was able to find a treatment that keeps my blood counts within a healthy range without the debilitating side effects I experienced with hydroxyurea. I think I have the same fatigue any other 66-year-old who travels for work all over the country would feel — which would not be possible if I hadn't spoken up."

About Jakafi

Jakafi can cause serious side effects including low blood counts and infection. Some people who take Jakafi have developed certain types of non-melanoma skin cancers. Increases in blood cholesterol levels can also occur. In patients who took another JAK inhibitor to treat rheumatoid arthritis, there was an increased risk of potentially fatal cardiovascular events like heart attack or stroke in patients with risk factors for these events who smoke now or smoked in the past, as well as an increased risk of blood clots in legs or lungs and new (secondary) cancers like lymphoma, especially in patients who smoke now or smoked in the past. The most common side effects of Jakafi for certain types of MF and polycythemia vera include: low platelet or red blood cell counts, bruising, dizziness, headache, and diarrhea.

Call your Health Care Professional for medical advice about side effects.

‌ To learn more about these and other risks, please read the Important Safety Information below and click for Full Prescribing Information for Jakafi. ‌

2. Do Your Research

When Donna was first diagnosed with PV, she began researching the condition on credible health websites, watching webinars from noted physicians around the country and learning more from her own doctors.

In her research, she took the time to understand the signs and symptoms, as well as what treatment options are available.

Donna brought up Jakafi to her oncologist when the hydroxyurea was making her feel sicker than ever, and they agreed Jakafi would be a good option for her.

"Within two weeks I noticed my body aches from my HU starting to improve," Donna says. "I started to be able to walk from my house to my mailbox. When I made it to the mailbox the first day I thought, 'OK, this is a small win I should celebrate.' It was a measurable improvement."

3. Advocating for Yourself Is Empowering (and Essential)

Doing her research via credible sources gave Donna the confidence to be honest with her health care providers when she felt like something was off, and the knowledge to discuss potential options with them.

"Patients not only know better than anyone else how they are feeling, they know about their experience with the condition in all the moments when they are not in the clinic being observed by the care team. They bring that expertise to the discussion with the health care provider when they decide together what to do next regarding treatment," Squier says. "This is true for all conditions but especially with diseases as rare, symptomatic and individual as PV."

"If I hadn't been an advocate for my own health, we probably wouldn't be having this conversation today," Donna says. "So, I say to everyone, be your own strong voice. Do not be intimidated by the medical profession. Know that your life is valuable, and you are responsible for your own health."

By working with her doctors and taking an active role in her health, Donna was able to find the treatment that makes her feel like her most vibrant self. Click here to hear more about her journey.

To learn more, visit The Purple Chair , a series that explores the emotional experiences of individuals from diagnosis through to the discovery of a path forward with Jakafi.

Please read the Important Safety Information below and click for ‌ Full Prescribing Information ‌.

‌ Indications and Usage ‌

Jakafi is a prescription medicine used to treat adults with polycythemia vera who have already taken a medicine called hydroxyurea and it did not work well enough or they could not tolerate it.

Jakafi is used to treat adults with certain types of myelofibrosis.

Jakafi is used to treat adults and children 12 years of age and older with acute graft-versus-host disease (GVHD) who have taken corticosteroids and they did not work well enough.

Jakafi is also used to treat adults and children 12 years of age and older with chronic GVHD who have taken one or two types of treatments and they did not work well enough.

‌ IMPORTANT SAFETY INFORMATION ‌

‌ Jakafi can cause serious side effects, including: ‌

‌ Low blood counts: ‌ Jakafi® (ruxolitinib) may cause low platelet, red blood cell, and white blood cell counts. If you develop bleeding, stop taking Jakafi and call your health care provider. Your health care provider will do a blood test to check your blood counts before you start Jakafi and regularly during your treatment. Your health care provider may change your dose of Jakafi or stop your treatment based on the results of your blood tests. Tell your health care provider right away if you develop or have worsening symptoms such as unusual bleeding, bruising, tiredness, shortness of breath, or a fever.

‌ Infection ‌: You may be at risk for developing a serious infection during treatment with Jakafi. Tell your health care provider if you develop any of the following symptoms of infection: chills, nausea, vomiting, aches, weakness, fever, painful skin rash or blisters.

‌ Cancer: ‌ Some people have had certain types of non-melanoma skin cancers during treatment with Jakafi. Your health care provider will regularly check your skin during your treatment with Jakafi. Tell your health care provider if you develop any new or changing skin lesions during treatment with Jakafi.

‌ Increases in cholesterol: ‌ You may have changes in your blood cholesterol levels during treatment with Jakafi. Your health care provider will do blood tests to check your cholesterol levels about every 8 to 12 weeks after you start taking Jakafi, and as needed.

‌ Increased risk of major cardiovascular events such as heart attack, stroke or death in people who have cardiovascular risk factors and who are current or past smokers while using another JAK inhibitor to treat rheumatoid arthritis: ‌ Get emergency help right away if you have any symptoms of a heart attack or stroke while taking Jakafi, including: discomfort in the center of your chest that lasts for more than a few minutes, or that goes away and comes back, severe tightness, pain, pressure, or heaviness in your chest, throat, neck, or jaw, pain or discomfort in your arms, back, neck, jaw, or stomach, shortness of breath with or without chest discomfort, breaking out in a cold sweat, nausea or vomiting, feeling lightheaded, weakness in one part or on one side of your body, slurred speech

‌ Increased risk of blood clots: ‌ Blood clots in the veins of your legs (deep vein thrombosis, DVT) or lungs (pulmonary embolism, PE) have happened in people taking another JAK inhibitor for rheumatoid arthritis and may be life-threatening. Tell your health care provider right away if you have any signs and symptoms of blood clots during treatment with Jakafi, including: swelling, pain, or tenderness in one or both legs, sudden, unexplained chest or upper back pain, shortness of breath or difficulty breathing

‌ Possible increased risk of new (secondary) cancers: ‌ People who take another JAK inhibitor for rheumatoid arthritis have an increased risk of new (secondary) cancers, including lymphoma and other cancers. People who smoke or who smoked in the past have an added risk of new cancers.

‌ The most common side effects of Jakafi include: ‌ for certain types of myelofibrosis (MF) and polycythemia vera (PV) – low platelet or red blood cell counts, bruising, dizziness, headache, and diarrhea; for acute GVHD – low platelet counts, low red or white blood cell counts, infections, and swelling; and for chronic GVHD – low red blood cell or platelet counts and infections including viral infections.

These are not all the possible side effects of Jakafi. Ask your pharmacist or health care provider for more information. Call your doctor for medical advice about side effects.

‌ Before taking Jakafi, tell your health care provider about: ‌ all the medications, vitamins, and herbal supplements you are taking and all your medical conditions, including if you have an infection, have or had low white or red blood cell counts, have or had tuberculosis (TB) or have been in close contact with someone who has TB, had shingles (herpes zoster), have or had hepatitis B, have or had liver or kidney problems, are on dialysis, have high cholesterol or triglycerides, had cancer, are a current or past smoker, had a blood clot, heart attack, other heart problems or stroke, or have any other medical condition. Take Jakafi exactly as your health care provider tells you. Do not change your dose or stop taking Jakafi without first talking to your health care provider.

Women should not take Jakafi while pregnant or planning to become pregnant. Do not breastfeed during treatment with Jakafi and for 2 weeks after the final dose.

‌ Please see the accompanying ‌ ‌ Full Prescribing Information ‌ ‌ , which includes a more complete discussion of the risks associated with Jakafi. ‌

You are encouraged to report negative side effects of prescription drugs to the FDA. Visit ‌ www.fda.gov/medwatch ‌ , or call ‌ 1-800-FDA-1088 ‌.

You may also report side effects to Incyte Medical Information at 1-855-463-3463.

Incyte and the Incyte logo are registered trademarks of Incyte.

Jakafi and the Jakafi logo are registered trademarks of Incyte.

© 2024, Incyte. MAT-JAK-04976 03/24

‌ *Patient's last name has been redacted to respect her privacy. ‌

• Leukemia & Lymphoma Society: "Myeloproliferative Neoplasms (MPN) Research Funded by LLS"
• MPN Research Foundation: Understanding MPNs

Is this an emergency? If you are experiencing serious medical symptoms, please see the National Library of Medicine’s list of signs you need emergency medical attention or call 911.

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• National Cancer Awareness Day: Empowering Hope and Health

Coveted as one of the most notorious diseases in the world, cancer has known to be one of the leading causes of death across the world. Cancer in any form is life-threatening and people often shy away from discussing it. However, cancer awareness can be of great benefit to the common people.

Long Essay on Cancer

In this long essay on cancer, we are providing you with cancer meaning, speech on cancer awareness. Go through this cancer essay to get a complete overview of this deadly disease.

In a recent study conducted in 2018, it was found that around 9.5 million people died that year owing to cancer. The World Health Organisation has revealed that cancer is the second leading cause of death across the world. The statistics in India are also no better and as per recent figures about 1300 people die every day owing to cancer of different types. Cancer types and causes have seen a steady increase in the past decade which does not bode well for the world population.

Meaning of Cancer

Before we proceed in this essay on cancer, we must understand cancer's meaning or what exactly is cancer? Cancer is the term given collectively to any and all forms of unregulated cell growth. Normally, the cells inside our body follow a definitive cycle from generation to death. However, in a person suffering from cancer, this cycle is unchecked and hence the cell cycle passes through the checkpoints unhinged and the cells continue to grow.

Types of Cancer

Now, that we have a preliminary understanding of the meaning of cancer, let us proceed to the cancer types or specifications. Cancer types are usually named after the area they affect in the body - usually like skin, lung, pancreas, blood, stomach among the others. However, if classified biologically, there are primarily five types of cancer. These include - leukemia, melanoma, carcinoma, sarcoma, and lymphoma.

Leukemia is the type of cancer that originates in the blood marrow and is a cancer of the blood. In this cancer type, no tumors are formed. Melanoma is regarded as one of the most dangerous types of cancer as in this, the skin coloring pigment or melanin becomes cancerous in nature. Carcinomas are cancers of the various types of glands or organs such as the breasts, stomach, lungs, pancreas, etc. Cancers of the connective tissues such as the bones, muscles, etc are classified as sarcomas. Lymphomas, on the other hand, are cancers of the white blood cells. Among the most diagnosed types of cancers are carcinomas.

Cancer Causes

In the present day living environment, a number of factors are liable to cause cancer. However, in many cases, one single factor cannot be attributed or held responsible for causing cancer in an individual. The substances that are known to be cancer-causing or increasing the risks of cancer are known as carcinogens. Carcinogens can range from anything from pollutants to tobacco to something as simple as processed meats.

The effect of carcinogens, however, on different individuals is different and it is also dependent on a number of factors, be it physical, lifestyle-choice, or biological. The physical factors enabling the effect of carcinogens include exposure to different environmental conditions such as UV rays, X-rays, etc. Cancer among mining workers because of their constant exposure to asbestos and fine silicone dust is common. Biological factors generally include hereditary factors, such as the passing of a mutated BRCA1 or 2 mutations from mother to daughter in case of breast cancer. In addition, they also include factors such as age, gender, blood type, etc. Lifestyle choice refers to habits such as smoking, drinking, radiation exposure, etc, which can act as triggers for carcinogens.

Cancer Treatment

In this segment of our essay on cancer, we will discuss the various types of cancer treatments involved and their applicability. The most commonly applied cancer treatments include surgery, chemotherapy, and radiation therapy. Often, these treatments are given in a combination of one with the other. Surgery is usually performed in the case of benign tumors usually followed by a short cycle of preventive chemotherapy. The treatment of chemotherapy includes a combination of drugs targeted to kill cancer cells. Radiation therapy, on the other hand, makes use of radiations to kill cancerous cells. All these treatments are usually known to have side effects, so after-care for cancer survivors is also equally important.

The kind of treatment best suited for a patient is usually determined by the physician. The most important aspect of cancer treatment is early diagnosis and immediate medical intervention. The chances of surviving or beating cancer increase by a paramount value if diagnosed in the early stages.

Cancer Awareness

In India, and many other countries, speaking or discussing cancer is still considered taboo and this perception is in dire need of a change. Always remember cancer awareness is the first step towards cancer prevention. You must come across survivors sharing their journey by means of speech of cancer awareness. It can be of great benefit to know about the disease beforehand as it will keep you wary of any signs or symptoms you might come across and bring the same to the notice of your physician immediately. This will help in preventing or fighting cancer more effectively.

Short Essay on Cancer

To provide you with a grasp on the subject matter, we have provided a short essay on cancer here. Cancer is a disease in which the cells in specified or different parts of the body start dividing continuously. Cancer is usually caused by specific substances that affect several factors in our body. These specific substances are called carcinogens.

Cancer can be caused owing to exposure to pollution, radiation, harmful substances, poor lifestyle choices, etc. Cancer is best treated when detected early. Usually, surgery as well as other treatments such as chemotherapy, radiation therapy, etc. are used to treat cancer.

Cancer awareness is one of the best means that help in preventing and fighting the disease.

Points to Remember About Cancer

Students are recommended to remember the point of facts so it can be helpful for the students to write an essay with ease. Below are listed a few quick points for the convenience of students who are opting to write an essay on Cancer—

Cancer is a condition in which the cells divide in vast numbers uncontrollably which results in impairment and other damage to the body.

Excessive alcohol consumption, poor nutrition or physical inactivity and, excess weight of the body are some of the causes of Cancer. 

Genetic factors can be responsible for the development of cancer. 

Some genetic malfunctions occur after birth and factors like exposure to the sun and smoking can increase the risks. 

A person can also inherit a certain predisposition for a particular type of cancer. 

Chemotherapy is one of the treatments for cancer that targets the dividing cells, it can cure cancer but the side effects can be fatal. 

Hormone Therapy is another way for treating cancer where the medication targets certain hormones that interfere with the human body. Hormones are essential in breast cancer and prostate cancer. 

Immunotherapy is another way where the medication and treatment target the immune system to boost it.

Personalized medication is one of the newer developments where the treatment is more personalized depending on the person’s body and gene. It is believed that this kind of treatment can cure all types of cancer. 

Radiation therapy is the treatment in which a high dose of radiation is given out to kill the cancerous cells. It can be used for shrinking the tumors before the surgery. 

Stem cell transplant is essential for blood-related cancer like leukemia and lymphoma. In this treatment, the blood cells are removed that are destroyed by chemotherapy and radiation and then the cells are put back into the body after being developed by the doctors. 

Surgery is also a part of the treatment. 

Leukemia, Breast cancer, thyroid cancer, melanoma, non-Hodgkin’s lymphoma, pancreatic, endometrial, colon, liver, and bladder cancer are the types of cancer that people are diagnosed with every year. 

The most common types of cancer are lung cancer and melanoma.

Cancer is classified by doctors in two ways. 

First, by the location of the cancerous cells. 

And secondly, by the tissues that are affected by it. 

Metastasis is a condition where cancerous cells spread to different parts of the body. 

Improvements in the rate of cancer have been seen over the years after a significant drop in tobacco consumption and smoking. 

The outlook of cancer depends on the severity, type, and location of the cancerous cells.  

Some cancer can exhibit symptoms while others don’t so it is always advised to report anything to the medical expert if something is wrong. Cancer doesn’t exhibit many symptoms unless it is in an advanced stage so it is usually better to go for regular checkups. 

Tumors can be caused in the brain and spinal that can be cancerous in nature. 

Germ cell tumors give rise to sperm and eggs in the body and it can be caused in any part of the body. 

Quick Ways to Remember and Write an Essay on Cancer

Do the research

It is essential to write the valid points and present them in this essay as it is based on Cancer. An essay on Cancer must be comprehensive and should ideally contain the context related to this topic hence, it is very important for a student to know about this topic thoroughly in order to write the essay brilliantly. 

Analyze the question

A student must understand the intention of the essay and know the terms that are needed to be used. It will clearly form an essay that consists of all the valid points related to cancer. 

Remembering the information on Cancer

Cancer as a topic is vast because there are several types of Cancer and writing about all of them is not possible in a condensed essay so it is important to understand and remember the points which are more essential than the others to be mentioned in the essay.  

Defining the terms and theories

It is essential for a student to explain the terms being used in the essay. For example, writing the names of the types of Cancer is not enough, it also has to be explained by the student on how it affects and how it may be treated. 

Organize a structured essay 

Students must write the essay in a coherent manner which must begin with the introduction to cancer, followed by the body of the essay that must contain the types of cancer, treatment, and other information regarding the topic of Cancer. It must be well concluded later to tie everything up neatly. 

Cancer is, undoubtedly, one of the most life-shattering diseases. Together, let us make an effort to take on this disease with more care and hope.

FAQs on National Cancer Awareness Day: Empowering Hope and Health

1. Differentiate Between Cancerous and Non-Cancerous Tumours.

The unregulated cell mass inside the body is known as a tumour and can be specified to a particular area or the uninhibited cell growth may spread to the surrounding tissues. Based on this, tumours are majorly classified into two types:

Benign Tumours: This type of tumours are usually regarded as non-cancerous as they are specified to a particular area and can be surgically removed without causing damage to the surrounding tissue.

Malignant Tumours: These tumours, on the other hand, have broken free from their site of origin and spread to other tissues, usually through the bloodstream. These tumours are cancerous in nature and usually require other treatments.

Cancer patients can now be 'matched' to best treatment with DNA and lab-dish experiments

Identifying the most effective cancer treatment for a given patient from the get-go can help improve outcomes.

Despite many efforts to find better, more effective ways to treat cancer, it remains a  leading cause of death by disease  among children in the U.S.

Cancer patients are also getting younger. Cancer diagnoses among those under 50 has risen by  about 80% worldwide  over the past 30 years. As of 2023, cancer is the  second-leading cause of death  both in the U.S. and around the world. While death rates from cancer have decreased over the past few decades,  about 1 in 3 patients in the U.S.  and  1 in 2 patients worldwide  still die from cancer.

Despite advances in standard cancer treatments, many cancer patients still face uncertain outcomes when these treatments prove ineffective. Depending on the stage and location of the cancer and the patient's medical history, most cancer types are treated with a mix of radiation, surgery and drugs. But if those standard treatments fail, patients and doctors enter a trial-and-error maze where effective treatments become difficult to predict because of limited information on the patient's cancer.

My mission as a  cancer researcher  is to build a personalized guide of the most effective drugs for every cancer patient. My team and I do this by testing different medications on a patient's own cancer cells before administering treatment, tailoring therapies that are most likely to selectively kill tumors while minimizing toxic effects.

In our newly published results of the first clinical trial combining drug sensitivity testing with DNA testing to identify effective treatments in children with cancer, an approach called  functional precision medicine , we found this approach  can help match patients  with more FDA-approved treatment options and significantly improve outcomes.

What is functional precision medicine?

Even though two people with the same cancer might get the same medicine, they can have very different outcomes. Because each patient's tumor is unique, it can be challenging to know which treatment works best.

To solve this problem, doctors analyze DNA mutations in the patient's tumor, blood or saliva to match cancer medicines to patients. This approach is called  precision medicine . However, the relationship between cancer DNA and how effective medicines will be against them is very complex. Matching medications to patients based on a single mutation overlooks other genetic and nongenetic mechanisms that influence how cells respond to drugs.

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How to best match medicines to patients through DNA is still a major challenge. Overall,  only 10% of cancer patients   experience a clinical benefit  from treatments matched to tumor DNA mutations.

Functional precision medicine takes a different approach to personalizing treatments. My team and I take a sample of a patient's cancer cells from a biopsy, grow the cells in the lab and expose them to over 100 drugs approved by the Food and Drug Administration. In this process, called  drug sensitivity testing , we look for the medications that kill the cancer cells.

New clinical trial results

Providing functional precision medicine to cancer patients  in real life  is very challenging. Off-label use of drugs and financial restrictions are key barriers. The health of cancer patients can also deteriorate rapidly, and physicians may be hesitant to try new methods.

But this is starting to change. Two teams in Europe recently showed that functional precision medicine could match effective treatments to  about 55% of   adult patients  with blood cancers such as leukemia and lymphoma that did not respond to standard treatments.

Most recently, my team's clinical trial  focused on childhood cancer patients  whose cancer came back or didn't respond to treatment. We applied our functional precision medicine approach to 25 patients with different types of cancer.

Our trial showed that we could provide treatment options for almost all patients in less than two weeks. My colleague  Arlet Maria Acanda de la Rocha  was instrumental in helping return drug sensitivity data to patients as fast as possible. We were able to provide test results within 10 days of receiving a sample, compared with the roughly 30 days that standard genomic testing results that focus on identifying specific cancer mutations typically take to process.

Most importantly, our study showed that  83% of cancer patients  who received treatments guided by our approach had clinical benefit, including improved response and survival.

Expanding into the real world

Functional precision medicine opens new paths to understanding how cancer drugs can be better matched to patients. Although doctors can read any patient's DNA today, interpreting the results to understand how a patient will respond to cancer treatment is much more challenging. Combining drug sensitivity testing with DNA analysis can help personalize cancer treatments for each patient.

I, along with colleague  Noah E. Berlow , have started to add artificial intelligence to our functional precision medicine program. AI enables us to analyze each patient's data to better match them with tailored treatments and drug combinations. AI also allows us to understand the complex relationships between DNA mutations within tumors and how different treatments will affect them.

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My team and I have  started two   clinical trials  to expand the results of our previous studies on providing treatment recommendations through functional precision medicine. We're recruiting a larger cohort of adults and children with cancers that have come back or are resistant to treatment.

The more data we have, the easier it will become to understand how to best treat cancer and ultimately help more patients access personalized cancer treatments.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article .

Diana Azzam is an Assistant Professor and Research Director of the newly established Center for Advancing Personalized Cancer Treatments (CAPCT) at Florida International University. She has a Masters in Biochemistry from the American University of Beirut, Lebanon and a PhD in Biochemistry & Molecular Biology from the University of Miami, Florida. Her lab focuses on implementing functional precision medicine (FPM) approaches in adult and pediatric cancer patients that have run out of treatment options. Working with local hospitals including Nicklaus Children's Hospital and Cleveland Clinic Florida, her lab delivers individualized treatment plans based on a patient's cancer genomic profile and ex vivo drug response. She is currently engaged in two clinical studies to assess feasibility and clinical utility of FPM in relapsed/refractory patients with childhood cancer (ClinicalTrials.gov registration: NCT05857969) and adult cancer (ClinicalTrials.gov registration: NCT06024603). She is working on setting up the first CLIA-certified lab in the State of Florida dedicated for functional cancer drug testing. Her goal is to launch large-scale prospective multi-center randomized clinical trials to better assess efficacy of FPM approaches in the treatment of refractory/relapsed cancers. In parallel, she is working on utilizing FPM as a tool to reduce health disparities in childhood cancer patients from minority populations. She is also integrating a novel machine learning approach to identify specific biomarkers among minority populations that can be targeted using FDA-approved drugs. Her lab also investigates cancer stem cells and how they may result from chronic environmental exposures to toxic metals such as arsenic.

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April 11, 2024

Scientists Found a Way to Supercharge Cancer-Fighting Cells

The bioengineered immune players called CAR T cells last longer and work better if pumped up with a large dose of a protein that makes them resemble stem cells

By Sara Reardon & Nature magazine

Alle abzählbaren Mengen haben ein Maß von null |

Um das zu sehen, kann man die Menge M = { m 1 , m 2 , m 3 , … , m i , ...} betrachten. Da M abzählbar viele Elemente enthält, kann man sie mit einem ganzzahligen Index i nummerieren. Um das Maß μ(M) zu bestimmen, kann man eine Abschätzung vornehmen. Dafür bildet man um jedes m i herum ein kleines Intervall I i mit abnehmender, beliebig kleiner Breite ε/(2 i ): I i = [ m i − ε⁄(2 i +1 ), m i + ε⁄(2 i +1 )] und bildet daraus eine neue Menge C = { I 1 , I 2 , I 3 , … , I i , …}.

C ähnelt also der ursprünglichen Menge , nur dass sie keine einzelnen Punkte m enthält, sondern kleine Intervalle. Insgesamt müsste das Maß von C also mindestens so groß sein wie das Maß von M: μ(M) ≤ μ(C). Nun lässt sich das Maß von C berechnen, indem man annimmt, dass ε so klein gewählt wird, damit sich die Intervalle I i niemals überlappen. Das Maß entspricht dann den addierten Längen der Intervalle: μ(C) = ∑ i ∞ ε/(2 i ) = ε. Damit folgt, dass das Maß von M kleiner gleich ε sein muss: μ(M) ≤ ε. Da ε aber beliebig klein gewählt werden kann, muss das Maß von M null ergeben. Damit ist bewiesen, dass für jede abzählbare Menge μ(M) = 0 gilt.

Thom Leach/Science Photo Library/Getty Images

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 .

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.

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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.

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. 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. 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 fought cancer without becoming exhausted. “It’s the ideal situation,” Darcy says.

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 to 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.

This article is reproduced with permission and was first published on April 10, 2024 .

BREAKING: Trump has arrived in the Manhattan courtroom as jury selection begins in his criminal trial

A quick test could protect against fatal chemo overdose, yet few doctors use it

One January morning in 2021, Carol Rosen took a standard treatment for metastatic breast cancer. Three gruesome weeks later, she died in excruciating pain from the very drug meant to prolong her life.

Rosen, a 70-year-old retired schoolteacher, passed her final days in anguish, enduring severe diarrhea and nausea and terrible sores in her mouth that kept her from eating, drinking, and, eventually, speaking. Skin peeled off her body. Her kidneys and liver failed. “Your body burns from the inside out,” said Rosen’s daughter, Lindsay Murray, of Andover, Massachusetts.

Rosen was one of more than 275,000 cancer patients in the United States who are infused each year with fluorouracil, known as 5-FU, or, as in Rosen’s case, take a nearly identical drug in pill form called capecitabine. These common types of chemotherapy are no picnic for anyone, but for patients who are deficient in an enzyme that metabolizes the drugs, they can be torturous or deadly.

Those patients essentially overdose because the drugs stay in the body for hours rather than being quickly metabolized and excreted. The drugs kill an estimated 1 in 1,000 patients who take them — hundreds each year — and severely sicken or hospitalize 1 in 50. Doctors can test for the deficiency and get results within a week — and then either switch drugs or lower the dosage if patients have a genetic variant that carries risk.

Yet a recent survey found that only 3% of U.S. oncologists routinely order the tests before dosing patients with 5-FU or capecitabine. That’s because the most widely followed U.S. cancer treatment guidelines — issued by the National Comprehensive Cancer Network — don’t recommend preemptive testing.

The FDA added new warnings about the lethal risks of 5-FU to the drug’s label on March 21 following queries from KFF Health News about its policy. However, it did not require doctors to administer the test before prescribing the chemotherapy.

The agency, whose plan to expand its oversight of laboratory testing was the subject of a House hearing , also March 21, has said it could not endorse the 5-FU toxicity tests because it’s never reviewed them.

But the FDA at present does not review most diagnostic tests, said Daniel Hertz, an associate professor at the University of Michigan College of Pharmacy. For years, with other doctors and pharmacists, he has petitioned the FDA to put a black box warning on the drug’s label urging prescribers to test for the deficiency.

“FDA has responsibility to assure that drugs are used safely and effectively,” he said. The failure to warn, he said, “is an abdication of their responsibility.”

The update is “a small step in the right direction, but not the sea change we need,” he said.

Europe ahead on safety

British and European Union drug authorities have recommended the testing since 2020. A small but growing number of U.S. hospital systems, professional groups, and health advocates, including the American Cancer Society, also endorse routine testing. Most U.S. insurers, private and public, will cover the tests, which Medicare reimburses for $175, although tests may cost more depending on how many variants they screen for.

In its latest guidelines on colon cancer, the Cancer Network panel noted that not everyone with a risky gene variant gets sick from the drug, and that lower dosing for patients carrying such a variant could rob them of a cure or remission. Many doctors on the panel, including the University of Colorado oncologist Dr. Wells Messersmith, have said they have never witnessed a 5-FU death.

In European hospitals, the practice is to start patients with a half- or quarter-dose of 5-FU if tests show a patient is a poor metabolizer, then raise the dose if the patient responds well to the drug. Advocates for the approach say American oncology leaders are dragging their feet unnecessarily, and harming people in the process.

“I think it’s the intransigence of people sitting on these panels, the mindset of ‘We are oncologists, drugs are our tools, we don’t want to go looking for reasons not to use our tools,’” said Gabriel Brooks, an oncologist and researcher at the Dartmouth Cancer Center.

Oncologists are accustomed to chemotherapy’s toxicity and tend to have a “no pain, no gain” attitude, he said. 5-FU has been in use since the 1950s.

Yet “anybody who’s had a patient die like this will want to test everyone,” said Dr. Robert Diasio of the Mayo Clinic, who helped carry out major studies of the genetic deficiency in 1988.

Oncologists often deploy genetic tests to match tumors in cancer patients with the expensive drugs used to shrink them. But the same can’t always be said for gene tests aimed at improving safety, said Mark Fleury, policy director at the American Cancer Society’s Cancer Action Network.

When a test can show whether a new drug is appropriate, “there are a lot more forces aligned to ensure that testing is done,” he said. “The same stakeholders and forces are not involved” with a generic like 5-FU, first approved in 1962 , and costing roughly $17 for a month’s treatment .

Oncology is not the only area in medicine in which scientific advances, many of them taxpayer-funded, lag in implementation. For instance, few cardiologists test patients before they go on Plavix, a brand name for the anti-blood-clotting agent clopidogrel, although it doesn’t prevent blood clots as it’s supposed to in a quarter of the 4 million Americans prescribed it each year. In 2021, the state of Hawaii won an $834 million judgment from drugmakers it accused of falsely advertising the drug as safe and effective for Native Hawaiians, more than half of whom lack the main enzyme to process clopidogrel.

The fluoropyrimidine enzyme deficiency numbers are smaller — and people with the deficiency aren’t at severe risk if they use topical cream forms of the drug for skin cancers. Yet even a single miserable, medically caused death was meaningful to the Dana-Farber Cancer Institute, where Carol Rosen was among more than 1,000 patients treated with fluoropyrimidine in 2021.

Her daughter was grief-stricken and furious after Rosen’s death. “I wanted to sue the hospital. I wanted to sue the oncologist,” Murray said. “But I realized that wasn’t what my mom would want.”

Instead, she wrote Dana-Farber’s chief quality officer, Dr. Joe Jacobson, urging routine testing. He responded the same day, and the hospital quickly adopted a testing system that now covers more than 90% of prospective fluoropyrimidine patients. About 50 patients with risky variants were detected in the first 10 months, Jacobson said.

Dana-Farber uses a Mayo Clinic test that searches for eight potentially dangerous variants of the relevant gene. Veterans Affairs hospitals use a 11-variant test, while most others check for only four variants.

Different tests may be needed for different ancestries

The more variants a test screens for, the better the chance of finding rarer gene forms in ethnically diverse populations. For example, different variants are responsible for the worst deficiencies in people of African and European ancestry, respectively. There are tests that scan for hundreds of variants that might slow metabolism of the drug, but they take longer and cost more.

These are bitter facts for Dr. Scott Kapoor, a Toronto-area emergency room physician whose brother, Dr. Anil Kapoor, died in February 2023 of 5-FU poisoning.

Anil Kapoor was a well-known urologist and surgeon, an outgoing speaker, researcher, clinician, and irreverent friend whose funeral drew hundreds. His death at age 58, only weeks after he was diagnosed with stage 4 colon cancer , stunned and infuriated his family.

In Ontario, where Kapoor was treated, the health system had just begun testing for four gene variants discovered in studies of mostly European populations. Anil Kapoor and his siblings, the Canadian-born children of Indian immigrants, carry a gene form that’s apparently associated with South Asian ancestry.

Scott Kapoor supports broader testing for the defect — only about half of Toronto’s inhabitants are of European descent — and argues that an antidote to fluoropyrimidine poisoning , approved by the FDA in 2015, should be on hand. However, it works only for a few days after ingestion of the drug and definitive symptoms often take longer to emerge.

Most importantly, he said, patients must be aware of the risk. “You tell them, ‘I am going to give you a drug with a 1 in 1,000 chance of killing you. You can take this test. Most patients would be, ‘I want to get that test and I’ll pay for it,’ or they’d just say, ‘Cut the dose in half.’”

Dr. Alan Venook, the University of California-San Francisco oncologist who co-chairs the National Comprehensive Cancer Network, has led resistance to mandatory testing because the answers provided by the test, in his view, are often murky and could lead to undertreatment.

“If one patient is not cured, then you giveth and you taketh away,” he said. “Maybe you took it away by not giving adequate treatment.”

Instead of testing and potentially cutting a first dose of curative therapy, “I err on the latter, acknowledging they will get sick,” he said. About 25 years ago, one of his patients died of 5-FU toxicity and “I regret that dearly,” he said. “But unhelpful information may lead us in the wrong direction.”

In September, seven months after his brother’s death, Kapoor was boarding a cruise ship on the Tyrrhenian Sea near Rome when he happened to meet a woman whose husband, Atlanta municipal judge Gary Markwell, had died the year before after taking a single 5-FU dose at age 77.

“I was like ... that’s exactly what happened to my brother.”

Murray senses momentum toward mandatory testing. In 2022, the Oregon Health & Science University paid $1 million to settle a suit after an overdose death.

“What’s going to break that barrier is the lawsuits, and the big institutions like Dana-Farber who are implementing programs and seeing them succeed,” she said. “I think providers are going to feel kind of bullied into a corner. They’re going to continue to hear from families and they are going to have to do something about it.”

Arthur Allen | KFF Health News

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Understanding cancer.

In simple terms, cancer is a group of more than 100 diseases that develop across time and involve the uncontrolled division of the body's cells. Although cancer can develop in virtually any of the body's tissues, and each type of cancer has its unique features, the basic processes that produce cancer are quite similar in all forms of the disease.

Cancer begins when a cell breaks free from the normal restraints on cell division and begins to follow its own agenda for proliferation ( Figure 3 ). All of the cells produced by division of this first, ancestral cell and its progeny also display inappropriate proliferation. A tumor , or mass of cells, formed of these abnormal cells may remain within the tissue in which it originated (a condition called in situ cancer), or it may begin to invade nearby tissues (a condition called invasive cancer). An invasive tumor is said to be malignant , and cells shed into the blood or lymph from a malignant tumor are likely to establish new tumors ( metastases ) throughout the body. Tumors threaten an individual's life when their growth disrupts the tissues and organs needed for survival.

The stages of tumor development. A malignant tumor develops across time, as shown in this diagram. This tumor develops as a result of four mutations, but the number of mutations involved in other types of tumors can vary. We do not know the exact number (more...)

What happens to cause a cell to become cancerous? Thirty years ago, scientists could not offer a coherent answer to this question. They knew that cancer arose from cells that began to proliferate uncontrollably within the body, and they knew that chemicals, radiation, and viruses could trigger this change. But exactly how it happened was a mystery.

Research across the last three decades, however, has revolutionized our understanding of cancer. In large part, this success was made possible by the development and application of the techniques of molecular biology, techniques that enabled researchers to probe and describe features of individual cells in ways unimaginable a century ago. Today, we know that cancer is a disease of molecules and genes, and we even know many of the molecules and genes involved. In fact, our increasing understanding of these genes is making possible the development of exciting new strategies for avoiding, forestalling, and even correcting the changes that lead to cancer.

• Unraveling the Mystery of Cancer

People likely have wondered about the cause of cancer for centuries. Its name derives from an observation by Hippocrates more than 2,300 years ago that the long, distended veins that radiate out from some breast tumors look like the limbs of a crab. From that observation came the term karkinoma in Greek, and later, cancer in Latin.

With the work of Hooke in the 1600s, and then Virchow in the 1800s, came the understanding that living tissues are composed of cells, and that all cells arise as direct descendants of other cells. Yet, this understanding raised more questions about cancer than it answered. Now scientists began to ask from what kinds of normal cells cancer cells arise, how cancer cells differ from their normal counterparts, and what events promote the proliferation of these abnormal cells. And physicians began to ask how cancer could be prevented or cured.

Clues from epidemiology

One of the most important early observations that people made about cancer was that its incidence varies between different populations. For example, in 1775, an extraordinarily high incidence of scrotal cancer was described among men who worked as chimney sweeps as boys. In the mid-1800s, lung cancer was observed at alarmingly high rates among pitch blende miners in Germany. And by the end of the 19th century, using snuff and cigars was thought by some physicians to be closely associated with cancers of the mouth and throat.

These observations and others suggested that the origin or causes of cancer may lie outside the body and, more important, that cancer could be linked to identifiable and even preventable causes. These ideas led to a widespread search for agents that might cause cancer. One early notion, prompted by the discovery that bacteria cause a variety of important human diseases, was that cancer is an infectious disease. Another idea was that cancer arises from the chronic irritation of tissues. This view received strong support with the discovery of X-rays in 1895 and the observation that exposure to this form of radiation could induce localized tissue damage, which could lead in turn to the development of cancer. A conflicting view, prompted by the observation that cancer sometimes seems to run in families, was that cancer is hereditary.

Such explanations, based as they were on fragmentary evidence and incomplete understanding, helped create the very considerable confusion about cancer that existed among scientists well into the mid-twentieth century. The obvious question facing researchers—and no one could seem to answer it—was how agents as diverse as this could all cause cancer. Far from bringing science closer to understanding cancer, each new observation seemed to add to the confusion.

Yet each new observation also, ultimately, contributed to scientists' eventual understanding of the disease. For example, the discovery in 1910 that a defined, submicroscopic agent isolated from a chicken tumor could induce new tumors in healthy chickens showed that a tumor could be traced simply and definitively back to a single cause. Today, scientists know this agent as Roussarcoma virus, one of several viruses that can act as causative factors in the development of cancer.

Although cancer-causing viruses are not prime agents in promoting most human cancers, their intensive study focused researchers' attention on cellular genes as playing a central role in the development of the disease.

Likewise, investigations into the association between cancer and tissue damage, particularly that induced by radiation, revealed that while visible damage sometimes occurs, something more subtle happens in cells exposed to cancer-causing agents. One clue to what happens came from the work of Herman Muller, who noticed in 1927 that X-irradiation of fruit flies often resulted in mutant offspring. Might the two known effects of X-rays, promotion of cancer and genetic mutation, be related to one another? And might chemical carcinogens induce cancer through a similar ability to damage genes?

Support for this idea came from the work of Bruce Ames and others who showed in 1975 that com pounds known to be potent carcinogens (cancer-causing agents) generally also were potent mutagens (mutation-inducing agents), and that compounds known to be only weak carcinogens were only weak mutagens. Although scientists know today that many chemicals do not follow this correlation precisely, this initial, dramatic association between mutagenicity and carcinogenicity had widespread influence on the development of a unified view of the origin and development of cancer.

Finally, a simple genetic model, proposed by Alfred Knudson in 1971, provided both a compelling explanation for the origins of retinoblastoma, a rare tumor that occurs early in life, and a convincing way to reconcile the view of cancer as a disease produced by external agents that damage cells with the observation that some cancers run in families. Knudson's model states that children with sporadic retinoblastoma (children whose parents have no history of the disease) are genetically normal at the moment of conception, but experience two somatic mutations that lead to the development of an eye tumor. Children with familial retinoblastoma (children whose parents have a history of the disease) already carry one mutation at conception and thus must experience only one more mutation to reach the doubly mutated configuration required for a tumor to form. In effect, in familial retinoblastoma, each retinal cell is already primed for tumor development, needing only a second mutational event to trigger the cancerous state. The difference in probabilities between the requirement for one or two mutational events, happening randomly, explains why in sporadic retinoblastoma, the affected children have only one tumor focus, in one eye, while in familial retinoblastoma, the affected children usually have multiple tumor foci growing in both eyes.

Although it was years before Knudson's explanation was confirmed, it had great impact on scientists' understanding of cancer. Retinoblastoma, and by extension, other familial tumors, appeared to be linked to the inheritance of mutated versions of growth-suppressing genes. This idea led to the notion that cells in sporadically arising tumors might also have experienced damage to these critical genes as the cells moved along the path from the normal to the cancerous state.

Clues from cell biology

Another field of study that contributed to scientists' growing understanding of cancer was cell biology. Cell biologists studied the characteristics of cancer cells, through observations in the laboratory and by inferences from their appearance in the whole organism. Not unexpectedly, these investigations yielded a wealth of information about normal cellular processes. But they also led to several key understandings about cancer, understandings that ultimately allowed scientists to construct a unified view of the disease.

One such understanding is that cancer cells are indigenous cells—abnormal cells that arise from the body's normal tissues. Furthermore, virtually all malignant tumors are monoclonal in origin, that is, derived from a single ancestral cell that somehow underwent conversion from a normal to a cancerous state. These insights, as straight for ward as they seem, were surprisingly difficult to reach. How could biologists describe the cell pedigree of a mass of cells that eventually is recognized as a tumor?

One approach to identifying the origin of cancer cells came from attempts to transplant tissues from one person to another. Such transplants work well between identical twins, but less well as the people involved are more distantly related. The barrier to successful transplantation exists because the recipient's immune system can distinguish between cells that have always lived inside the self and cells of foreign origin. One practical application of this discovery is that tissues can be classified as matching or nonmatching before a doctor attempts to graft a tissue or organ into another person's body. Such tissue-typing tests, when done on cancer cells, reveal that the tumor cells of a particular cancer patient are always of the same transplantation type as the cells of normal tissues located elsewhere in the person's body. Tumors, therefore, arise from one's own tissues, not from cells introduced into the body by infection from another person.

How do we know that tumors are monoclonal? Two distinct scenarios might explain how cancers develop within normal tissues. In the first, many individual cells become cancerous, and the resulting tumor represents the descendants of these original cells. In this case, the tumor is polyclonal in nature ( Figure 4 ). In the second scenario, only one cell experiences the original transformation from a normal cell to a cancerous cell, and all of the cells in the tumor are descendants of that cell.

Two schemes by which tumors can develop. Most—if not all—human cancer appears to be monoclonal.

Direct evidence supporting the monoclonal origin of virtually all malignant tumors has been difficult to acquire because most tumor cells lack obvious distinguishing marks that scientists can use to demonstrate their clonal relationship. There is, however, one cellular marker that scientists can use as an indication of such relationships: the inactivated X chromosome that occurs in almost all of the body cells of a human female. X-chromosome inactivation occurs randomly in all cells during female embryonic development. Because the inactivation is random, the female is like a mosaic in terms of the X chromosome, with different copies of the X turned on or off in different cells of the body. Once inactivation occurs in a cell, all of the future generations of cells coming from that cell have the same chromosome inactivated in them as well (either the maternal or the paternal X). The observation that all the cells within a given tumor invariably have the same X chromosome inactivated suggests that all cells in the tumor must have descended from a single ancestral cell.

Cancer, then, is a disease in which a single normal body cell undergoes a genetic transformation into a cancer cell. This cell and its descendants, proliferating across many years, produce the population of cells that we recognize as a tumor, and tumors produce the symptoms that an individual experiences as cancer.

Even this picture, although accurate in its essence, did not represent a complete description of the events involved in tumor formation. Additional research revealed that as a tumor develops, the cells of which it is composed become different from one another as they acquire new traits and form distinct subpopulations of cells within the tumor. As shown in Figure 5 , these changes allow the cells that experience them to compete with increasing success against cells that lack the full set of changes. The development of cancer, then, occurs as a result of a series of clonal expansions from a single ancestral cell.

A series of changes leads to tumor formation. Tumor formation occurs as a result of successive clonal expansions. This figure illustrates only three such changes; the development of many cancers likely involves more than three.

A second critical understanding that emerged from studying the biology of cancer cells is that these cells show a wide range of important differences from normal cells. For example, cancer cells are genetically unstable and prone to rearrangements, duplications, and deletions of their chromosomes that cause their progeny to display unusual traits. Thus, although a tumor as a whole is monoclonal in origin, it may contain a large number of cells with diverse characteristics.

Cancerous cells also look and act differently from normal cells. In most normal cells, the nucleus is only about one-fifth the size of the cell; in cancerous cells, the nucleus may occupy most of the cell's volume. Tumor cells also often lack the differentiated traits of the normal cell from which they arose. Whereas normal secretory cells pro duce and release mucus, cancers derived from these cells may have lost this characteristic. Likewise, epithelial cells usually contain large amounts of keratin, but the cells that make up skin cancer may no longer accumulate this protein in their cytoplasms.

The key difference between normal and cancerous cells, however, is that cancer cells have lost the restraints on growth that characterize normal cells. Significantly, a large number of cells in a tumor are engaged in mitosis, whereas mitosis is a relatively rare event in most normal tissues. Cancer cells also demonstrate a variety of unusual characteristics when grown in culture; two such examples are a lack of contact inhibition and a reduced dependence on the presence of growth factors in the environment. In contrast to normal cells, cancer cells do not cooperate with other cells in their environment. They often proliferate indefinitely in tissue culture. The ability to divide for an apparently unlimited number of generations is another important characteristic of the cancerous state, allowing a tumor composed of such cells to grow without the constraints that normally limit cell growth.

A unified view

By the mid-1970s, scientists had started to develop the basis of our modern molecular understanding of cancer. In particular, the relationship Ames and others had established between mutagenicity and carcinogenicity pro vided substantial support for the idea that chemical carcinogens act directly through their ability to damage cellular genes. This idea led to a straightforward model for the initiation of cancer: Carcinogens induce mutations in critical genes, and these mutations direct the cell in which they occur, as well as all of its progeny cells, to grow abnormally. The result of this abnormal growth appears years later as a tumor. The model could even explain the observation that cancer sometimes appears to run in families: If cancer is caused by mutations in critical genes, then people who inherit such mutations would be more susceptible to cancer's development than people who do not.

As exciting as it was to see a unified view of cancer begin to emerge from the earlier confusion, cancer researchers knew their work was not finished. The primary flaw in their emerging explanation was that the nature of these cancer-causing mutations was unknown. Indeed, their very existence had yet to be proven. Evidence from work with cancer-causing viruses suggested that only a small number of genes were involved, and evidence from cell biology pointed to genes that normally control cell division. But now scientists asked new questions: Exactly which genes are involved? What are their specific roles in the cell? and How do their functions change as a result of mutation?

It would take another 20 years and a revolution in the techniques of biological research to answer these questions. However, today our picture of the causes and development of cancer is so detailed that scientists find themselves in the extraordinary position of not only knowing many of the genes involved but also being able to target prevention, detection, and treatment efforts directly at these genes.

• Cancer as a Multistep Process

A central feature of today's molecular view of cancer is that cancer does not develop all at once, but across time, as a long and complex succession of genetic changes. Each change enables precancerous cells to acquire some of the traits that together create the malignant growth of cancer cells.

Two categories of genes play major roles in triggering cancer. In their normal forms, these genes control the cell cycle , the sequence of events by which cells enlarge and divide. One category of genes, called proto-oncogenes , encourages cell division. The other category, called tumor suppressor genes , inhibits it. Together, proto-oncogenes and tumor suppressor genes coordinate the regulated growth that normally ensures that each tissue and organ in the body maintains a size and structure that meets the body's needs.

What happens when proto-oncogenes or tumor suppressor genes are mutated? Mutated proto oncogenes become oncogenes, genes that stimulate excessive division. And mutations in tumor suppressor genes inactivate these genes, eliminating the critical inhibition of cell division that normally prevents excessive growth. Collectively, mutations in these two categories of genes account for much of the uncontrolled cell division that occurs in human cancers ( Figure 6 ).

Some Genes Involved in Human Cancer

The role of oncogenes

How do proto-oncogenes, or more accurately, the oncogenes they become after mutation, contribute to the development of cancer? Most proto-oncogenes code for proteins that are involved in molecular pathways that receive and process growth-stimulating signals from other cells in a tissue. Typically, such signaling begins with the production of a growth factor, a protein that stimulates division. These growth factors move through the spaces between cells and attach to specific receptor proteins located on the surfaces of neighboring cells. When a growth-stimulating factor binds to such a receptor, the receptor conveys a stimulatory signal to proteins in the cytoplasm. These proteins emit stimulatory signals to other proteins in the cell until the division-promoting message reaches the cell's nucleus and activates a set of genes that help move the cell through its growth cycle.

Oncogenes, the mutated forms of these proto oncogenes, cause the proteins involved in these growth-promoting pathways to be overactive. Thus, the cell proliferates much faster than it would if the mutation had not occurred. Some oncogenes cause cells to overproduce growth factors. These factors stimulate the growth of neighboring cells, but they also may drive excessive division of the cells that just produced them. Other oncogenes produce aberrant receptor proteins that release stimulatory signals into the cytoplasm even when no growth factors are present in the environment. Still other oncogenes disrupt parts of the signal cascade that occurs in a cell's cytoplasm such that the cell's nucleus receives stimulatory messages continuously, even when growth factor receptors are not prompting them.

The role of tumor suppressor genes

To become cancerous, cells also must break free from the inhibitory messages that normally counterbalance these growth-stimulating pathways. In normal cells, inhibitory messages flow to a cell's nucleus much like stimulatory messages do. But when this flow is interrupted, the cell can ignore the normally powerful inhibitory messages at its surface.

Scientists are still trying to identify the normal functions of many known tumor suppressor genes. Some of these genes apparently code for proteins that operate as parts of specific inhibitory pathways. When a mutation causes such proteins to be inactivate or absent, these inhibitory pathways no longer function normally. Other tumor suppressor genes appear to block the flow of signals through growth-stimulating pathways; when these genes no longer function properly, such growth-promoting pathways may operate without normal restraint. Mutations in all tumor suppressor genes, however, apparently inactivate critical tumor suppressor proteins, depriving cells of this restraint on cell division.

The body's back-up systems

In addition to the controls on proliferation afforded by the coordinated action of proto-oncogenes and tumor suppressor genes, cells also have at least three other systems that can help them avoid runaway cell division. The first of these systems is the DNA repair system. This system operates in virtually every cell in the body, detecting and correcting errors in DNA. Across a lifetime, a person's genes are under constant attack, both by carcinogens imported from the environment and by chemicals produced in the cell itself. Errors also occur during DNA replication. In most cases, such errors are rapidly corrected by the cell's DNA repair system. Should the system fail, however, the error (now a mutation) becomes a permanent feature in that cell and in all of its descendants.

The system's normally high efficiency is one reason why many years typically must pass before all the mutations required for cancer to develop occur together in one cell. Mutations in DNA repair genes themselves, however, can undermine this repair system in a particularly devastating way: They damage a cell's ability to repair errors in its DNA. As a result, mutations appear in the cell (including mutations in genes that control cell growth) much more frequently than normal.

A second cellular back-up system prompts a cell to commit suicide (undergo apoptosis ) if some essential component is damaged or its control system is deregulated. This observation suggests that tumors arise from cells that have managed to evade such death. One way of avoiding apoptosis involves the p53 protein. In its normal form, this protein not only halts cell division, but induces apoptosis in abnormal cells. The product of a tumor suppressor gene, p53 is inactivated in many types of cancers.

This ability to avoid apoptosis endangers cancer patients in two ways. First, it contributes to the growth of tumors. Second, it makes cancer cells resistant to treatment. Scientists used to think that radiation and chemotherapeutic drugs killed cancer cells directly by harming their DNA. It seems clear now that such therapy only slightly damages the DNA in cells; the damaged cells, in response, actively kill themselves. This discovery suggests that cancer cells able to evade apoptosis will be less responsive to treatment than other cells.

A third back-up system limits the number of times a cell can divide, and so assures that cells cannot reproduce endlessly. This system is governed by a counting mechanism that involves the DNA segments at the ends of chromosomes. Called telomeres, these segments shorten each time a chromo some replicates. Once the telomeres are shorter than some threshold length, they trigger an internal signal that causes the cell to stop dividing. If the cells continue dividing, further shortening of the telomeres eventually causes the chromosomes to break apart or fuse with one another, a genetic crisis that is inevitably fatal to the cell.

Early observations of cancer cells grown in culture revealed that, unlike normal cells, cancer cells can proliferate indefinitely. Scientists have recently discovered the molecular basis for this characteristic—an enzyme called telomerase, that systematically replaces telomeric segments that are trimmed away during each round of cell division. Telomerase is virtually absent from most mature cells, but is present in most cancer cells, where its action enables the cells to proliferate endlessly.

The multistep development of cancer

Cancer, then, does not develop all at once as a massive shift in cellular functions that results from a mutation in one or two wayward genes. Instead, it develops step-by-step, across time, as an accumulation of many molecular changes, each contributing some of the characteristics that eventually pro duce the malignant state. The number of cell divisions that occur during this process can be astronomically large—human tumors often become apparent only after they have grown to a size of 10 billion to 100 billion cells. As you might expect, the time frame involved also is very long— it normally takes decades to accumulate enough mutations to reach a malignant state.

Understanding cancer as a multistep process that occurs across long periods of time explains a number of long-standing observations. A key observation is the increase in incidence with age. Cancer is, for the most part, a disease of people who have lived long enough to have experienced a complex and extended succession of events. Because each change is a rare accident requiring years to occur, the whole process takes a very long time, and most of us die from other causes before it is complete.

Understanding cancer in this way also explains the increase in cancer incidence in people who experience unusual exposure to carcinogens, as well as the increased cancer risk of people who inherit predisposing mutations. Exposure to carcinogens increases the likelihood that certain harmful changes will occur, greatly increasing the probability of developing cancer during a normal life span. Similarly, inheriting a cancer -susceptibility mutation means that instead of that mutation being a rare event, it already has occurred, and not just in one or two cells, but in all the body's cells. In other words, the process of tumor formation has leapfrogged over one of its early steps. Now the accumulation of changes required to reach the malignant state, which usually requires several decades to occur, may take place in one or two.

Finally, understanding the development of cancer as a multistep process also explains the lag time that often separates exposure to a cancer-causing agent and the development of cancer. This explains, for example, the observation that severe sunburns in children can lead to the development of skin cancer decades later. It also explains the 20-to 25-year lag between the onset of widespread cigarette smoking among women after World War II and the massive increase in lung cancer that occurred among women in the 1970s.

• The Human Face of Cancer

For most Americans, the real issues associated with cancer are personal. More than 8 million Americans alive today have a history of cancer (National Cancer Institute, 1998; Rennie, 1996). In fact, cancer is the second leading cause of death in the United States, exceeded only by heart disease.

Who are these people who develop cancer and what are their chances for surviving it? Scientists measure the impact of cancer in a population by looking at a combination of three elements: (1) the number of new cases per year per 100,000 persons ( incidence rate ), (2) the number of deaths per 100,000 persons per year ( mortality rate ), and (3) the proportion of patients alive at some point after their diagnosis of cancer ( survival rate ). Data on incidence, mortality, and survival are collected from a variety of sources. For example, in the United States there are many statewide cancer registries and some regional registries based on groups of counties, many of which surround large metropolitan areas. Some of these population-based registries keep track of cancer incidence in their geographic areas only; others also collect follow-up information to calculate survival rates.

In 1973, the National Cancer Institute began the Surveillance, Epidemiology, and End Results (SEER) Program to estimate cancer incidence and patient survival in the United States. SEER collects cancer incidence data in 11 geographic areas and two supplemental registries, for a combined population of approximately 14 percent of the entire U.S. population. Data from SEER are used to track cancer incidence in the United States by primary cancer site, race, sex, age, and year of diagnosis. For example, Figure 7 shows SEER data for the age-adjusted cancer incidence rates for the 10 most common sites for Caucasian and African-American males and females for the period 1987–1991.

Age-Adjusted Cancer Incidence Rates, 1987–1991

Cancer among children is relatively rare. SEER data from 1991 showed an incidence of only 14.1 cases per 100,000 children under age 15. Nevertheless, after accidents, cancer is the second leading cause of childhood death in the United States. Leukemias (4.3 per 100,000) and cancer of the brain and other nervous system organs (3.4 per 100,000) account for more than one-half of the cancers among children.

Everyone is at some risk of developing cancer. Cancer researchers use the term lifetime risk to indicate the probability that a person will develop cancer over the course of a lifetime. In the United States, men have a 1 in 2 lifetime risk of developing cancer, and women have a 1 in 3 risk.

For a specific individual, however, the risk of developing a particular type of cancer may be quite different from his or her lifetime risk of developing any type of cancer. Relative risk compares the risk of developing cancer between persons with a certain exposure or characteristic and persons who do not have this exposure or characteristic. For example, a person who smokes has a 10- to 20-fold higher relative risk of developing lung cancer compared with a person who does not smoke. This means that a smoker is 10- to 20-times more likely to develop lung cancer than a nonsmoker.

Scientists rely heavily on epidemiology to help them identify factors associated with the development of cancer. Epidemiologists look for factors that are common to cancer victims' histories and lives and evaluate these factors in the light of current understandings of the disease. With enough study, researchers may assemble evidence that a particular factor "causes" cancer, that is, that exposure to it increases significantly the probability of the disease developing. Although this information cannot be used to predict what will happen to any one individual exposed to this risk factor, it can help people make choices that reduce their exposure to known carcinogens (cancer-causing agents) and increase the probability that if cancer develops, it will be detected early (for example, by getting regular check-ups and participating in cancer screening programs).

As noted above, hereditary factors also can contribute to the development of cancer. Some people are born with mutations that directly promote the unrestrained growth of certain cells or the occurrence of more mutations. These mutations, such as the mutation identified in the 1980s that causes retinoblastoma, confer a high relative cancer risk. Such mutations are rare in the population, however, accounting for the development of fewer than 5 percent of the cases of fatal cancer.

Hereditary factors also contribute to the development of cancer by dictating a person's general physiological traits. For example, a person with fair skin is more susceptible to the development of skin cancer than a person with a darker complexion. Likewise, a person whose body metabolizes and eliminates a particular carcinogen relatively inefficiently is more likely to develop types of cancer associated with that carcinogen than a person who has more efficient forms of the genes involved in that particular metabolic process. These inherited characteristics do not directly promote the development of cancer; each person, susceptible or not, still must be exposed to the related environ mental carcinogen for cancer to develop. Nevertheless, genes probably do contribute in some way to the vast majority of cancers.

One question often asked about cancer is "How many cases of cancer would be expected to occur naturally in a population of individuals who somehow had managed to avoid all environmental carcinogens and also had no mutations that predisposed them to developing cancer?" Comparing populations around the world with very different cancer patterns has led epidemiologists to suggest that perhaps only about 25 percent of all cancers are "hard core"—that is, would develop anyway, even in a world free of external influences. These cancers would occur simply because of the production of carcinogens within the body and because of the random occurrence of unrepaired genetic mistakes.

Although cancer continues to be a significant health issue in the United States, a recent report from the American Cancer Society (ACS), National Cancer Institute (NCI), and Centers for Disease Control and Prevention (CDC) indicates that health officials are making progress in controlling the disease. In a news bulletin released on 12 March 1998, the ACS, NCI, and CDC announced the first sustained decline in the cancer death rate, a turning point from the steady increase observed throughout much of the century. The report showed that after increasing 1.2 percent per year from 1973 to 1990, the incidence for all cancers combined declined an average of 0.7 percent per year from 1990 to 1995. The overall cancer death rate also declined by about 0.5 percent per year across this period.

The overall survival rate for all cancer sites combined also continues to increase steadily, from 49.3 percent in 1974–1976 to 53.9 percent in 1983–1990 ( Figure 8 ). In some cases—for example, among children age 15 and younger—survival rates have increased dramatically.

Five-Year Relative Survival Rates for Selected Cancer Sites, All Races

• New Hope for Treating Cancer

What explanation can we offer for the steady increase in survival rates among cancer patients? One answer likely is the improvements scientists have made in cancer detection. These improvements include a variety of new imaging techniques as well as blood and other tests that can help physicians detect and diagnose cancer early. Although many Americans regularly watch for the early symptoms of cancer, by the time symptoms occur many tumors already have grown quite large and may have metastasized. Likewise, many cancers have no symptoms. Clearly, great effort is needed to educate Americans that cancer screening (checking for cancer in people with no symptoms) is key to early detection.

Another explanation for increased survival is improved treatment. Today, the traditional workhorses of cancer treatment—surgery, radiation, and chemotherapy—are being used in ways that are increasingly specific to the type of cancer involved. In fact, many cases of cancer now are being fully cured.

But is this the best we can do? What will the future bring? Hellman and Vokes, in their 1996 article in Scientific American , note that war often serves as a metaphor for cancer research. In 1971, two days before Christmas, President Richard M. Nixon signed the National Cancer Act, committing the United States to a "war" on cancer. Although the analogy is not perfect, Hellman and Vokes suggest that it can help us understand our current position with respect to cancer prevention, detection, and treatment. Looking at the "map" of cancer research after almost 30 years of "war," we can see that we have made some modest advances. But these successes do not reveal the tremendous developments that lie ahead of us by virtue of the new, strategic position we have achieved. In fact, most scientists expect that our newly gained understanding of the molecular basis of cancer will eventually give rise to a whole generation of exciting new techniques, not only for detecting and treating cancer but also for preventing it.

A key area of interest lies in learning how to exploit the molecular abnormalities of cancer cells to bring about their destruction. For example, understanding the role of oncogenes in the development of cancer suggests new targets for anticancer therapies. Some drug companies are working on drugs designed to shut down abnormal receptor proteins. Other potential targets are the aberrant proteins within the cytoplasm that transmit stimulatory signals even without being stimulated by surface receptors.

As in the case of oncogenes, a better understanding of the role of tumor suppressor genes in preventing runaway cell division may help scientists develop new therapies directed at these genes. For example, various studies have shown that introducing a normal tumor suppressor gene into a cell can help restore the cell to normalcy. Similarly, a therapy capable of restoring a cell's capacity for apoptosis would improve significantly the effectiveness of current cancer treatments. Even telomerase represents an important potential target for scientists looking for new and more powerful treatments for cancer. If telomerase could be blocked in cancer cells, their telomeres would continue to shorten with each division until their own proliferation pushed them into a genetic crisis and death.

One bold new research initiative that offers significant promise is the Cancer Genome Anatomy Project (CGAP). The project's goal is to identify all the genes responsible for the establishment and growth of human cancer. The work is based on a simple concept: Although almost every cell in the body contains the full set of human genes, only about one-tenth of them are expressed in any particular type of cell. Thus, different types of cells— for example, muscle cells and skin cells—can be distinguished by their patterns of gene expression.

Establishing for a particular cell the repertoire of genes expressed, together with the amount of nor mal or altered gene product produced by each expressed gene, yields a powerful "fingerprint" or "signature" for that cell type. Not unexpectedly, during the transformation of a normal cell to a cancer cell, this signature changes. Some changes are quantitative. That is, gene A may be expressed in both cells, but at greatly different levels, or it may be expressed in one cell but not the other. Other changes are qualitative: Gene B may be expressed at the same level in both cells, but pro duce an altered product in the cancerous cell.

Scientists expect that being able to "read" these signatures—in other words, being able to compare the signatures of cells in their normal and cancerous states—will change cancer detection, diagnosis, and treatment in many exciting ways. Specifically, studying the exact sequence of molecular changes a cell undergoes during its transformation to a cancerous state will help scientists identify new molecular-level targets for prevention, detection, and treatment. One observation scientists have recently made is that cells surrounding an incipient tumor also may undergo changes that indicate that cancer is present. For example, early tobacco-induced molecular changes in the mouth may predict the risk of developing lung cancer, and cancers of the urinary tract may be signaled by molecularly-altered cells that are shed in the urine. Reading the signatures of these easily accessed cells may enable scientists to develop simple, non-invasive tests that will allow early detection of cancerous or precancerous cells hidden deep within the body.

Reading such signatures will also enhance the specificity of cancer diagnosis by allowing scientists to differentiate among tumors at the molecular level. By assessing the meaning of individual changes in a cell's signature, scientists will be able to determine which cancers are most likely to progress and which are not—a dilemma that confronts doctors in the treatment of prostate cancer—thereby allowing patients to avoid the harmful consequences of unnecessary treatment.

Finally, molecular fingerprinting will allow researchers to develop new treatments specifically targeted at cellular subtypes of different cancers. Often, patients suffering from tumors that by traditional criteria are indistinguishable, nevertheless experience quite different outcomes despite having received the same treatment. Research indicates that these different outcomes sometimes are related to the presence or absence of particular gene products. In the future, such molecular characteristics likely will be used to identify patients who would benefit from one type of treatment as compared with another.

The ultimate goal of such work, of course, is to push back the detection and diagnosis of cancer to its earliest stages of development. For the first time in the history of humankind, scientists can now envision the day when medical intervention for cancer will become focused at identifying incipient disease and preventing its progression to overt disease, rather than treating the cancer after it is well established.

• Cancer and Society

But what does this mean for society? The financial costs of cancer loom large, not only for the individual but also for the community. The NCI estimates overall annual costs for cancer at about $107 billion. This cost includes $37 billion for direct medical costs, $11 billion for morbidity costs (cost of lost productivity), and $59 billion for mortality costs. Interestingly, treatment for breast, lung, and prostate cancers account for more than one-half of the direct medical costs.

Although early detection and successful treatment can reduce cancer deaths, the most desirable way to reduce them is prevention. In fact, scientists estimate that as many as one-half of the deaths from cancer in the United States and Europe, two areas with closely tracked cancer rates, could theoretically be prevented.

Nevertheless, the widespread persistence of unhealthful habits suggests that many Americans remain unconvinced about the power of prevention as a defense against cancer. Part of the reason may be that the only data we have about factors related to cancer are drawn from whole populations. These data cannot tell us who will develop cancer. Nor can they tell us whether healthful choices prevented its appearance in a particular individual.

Unhealthful habits also may persist because of the long time that elapses between the exposures that trigger the development of cancer and its actual appearance as disease. Conversely, there is a time lag between the institution of a beneficial personal habit (such as quitting smoking) or public policy (such as banning use of a known carcinogen) and its positive impact on personal and public health.

In their article "Strategies for Minimizing Cancer Risk," Willett, Colditz, and Mueller propose four levels on which to focus cancer prevention efforts. The first level is that of the individual. These authors argue that because most of the actions that can prevent cancer must be taken by individuals, dissemination of accurate information directly to the American public, together with peer support for behavioral changes, are critical.

A second level is health care providers, who are in a position to provide both counseling and screening to individuals under their care. Here, dissemination of accurate and timely information also is key.

A third level of prevention is the national level, where government agencies can impose regulations that help minimize the public's exposure to known carcinogens and implement policies that improve public health. Examples include regulating industries to cease using potent carcinogens and providing community facilities for safe physical activity.

Finally, a fourth level of prevention is at the international level, where the actions of developed countries can affect the incidence of cancer worldwide. Unfortunate examples of this include promoting the exportation of tobacco products and moving hazardous manufacturing processes to unregulated developing countries.

How do we think about devising and implementing measures to improve personal and public health in a pluralist society? One way to address this question is by attending to the ethical and public policy issues raised by our understanding and treatment of cancer.

A history of severe sunburns is strongly linked to the development of skin cancer later in life.

Ethics is the study of good and bad, right and wrong. It has to do with the actions and character of individuals, families, communities, institutions, and societies. During the last 2,500 years, Western philosophy has developed a variety of powerful methods and a reliable set of concepts and technical terms for studying and talking about the ethical life. Generally speaking, we apply the terms "right" and "good" to actions and qualities that foster the interests of individuals, families, communities, institutions, and society. Here, an "interest" refers to a participant's share in a situation. The terms "wrong" or "bad" apply to actions and qualities that impair interests. Often there are competing, well-reasoned answers to questions about what is right and wrong and good and bad about an individual's or group's conduct or actions.

Ethical considerations are complex, multifaceted, and raise many questions. In the United States, for example, we value protecting individuals from preventable harms. We support restrictions on who can purchase cigarettes and where smoking can occur. We inform pregnant women of the risks of drinking and smoking. However, we also value individual freedom and autonomy. We do not ban cigarettes outright; instead, we allow individuals over 18 years of age to take personal risks and be exposed to the related consequences. We permit pregnant women to buy and use liquor and cigarettes.

The inevitability of ethical tradeoffs is not simply a mark of the discussions in the United States. When considering differing health policy issues between and among countries, one cannot avoid encountering a pluralism of ethical considerations. Developing countries, whose health standards often differ from those in the United States, provide different cultural approaches to cancer and different standards for marketing and using tobacco and other known carcinogens. These different approaches raise a variety of ethical questions. For example, is there any legal and ethical way for people in the United States to prevent the widespread use of tobacco in other countries, a practice that contributes to the rise of lung cancer worldwide? Is there any legal and ethical way to govern other choices of individuals (for example, poor diet and lack of exercise) that contribute to cancer?

Typically, answers to such questions all involve an appeal to values. A value is something that has significance or worth in a given situation. One of the exciting events to witness in any discussion in ethics in a pluralist society is the varying ways in which the individuals involved assign value to things, persons, and states of affairs. Examples of values that students may appeal to in discussions of ethical issues include autonomy, freedom, privacy, sanctity of life, protecting another from harm, promoting another's good, justice, fairness, relationships, scientific knowledge, and technological progress.

Acknowledging the complex, multifaceted nature of ethical discussions is not to suggest that "anything goes." Experts generally agree on the following features of ethics. First, ethics is a process of rational inquiry. It involves posing clearly formulated questions and seeking well-reasoned answers to those questions. Well-reasoned answers to ethical questions constitute arguments . Ethical analysis and argument, then, result from successful ethical inquiry.

Second, ethics requires a solid foundation of information and rigorous interpretation of that information. For example, one must have a solid understanding of cancer to discuss the ethics of requiring protective covering to be worn to prevent skin cancer. Ethics is not strictly a theoretical discipline but is concerned in vital ways with practical matters.

Third, because tradeoffs among interests are complex, constantly changing, and sometimes uncertain, there are often competing, well-reasoned answers to questions about what is right and wrong and good and bad. This is especially true in a pluralist society.

Public policy is a set of guidelines or rules that results from the actions or lack of actions of government entities. Government entities act by making laws. In the United States, laws can be made by each of the three branches of government: by legislatures (statutory law), by courts (case law), and by regulatory agencies (regulatory law). Regulatory laws are written by the executive branch of the government, under authorization by the legislative branch. All three types of law are pertinent to how we respond to cancer. When laws exist to regulate behavior, public policy is called de jure public policy.

Whether one makes public policy involves at least the following five considerations:

• -the costs of implementing particular policies (including financial, social, and personal costs),
• the urgency of implementing a new policy,
• how effective a particular policy is likely to be,
• -whether appropriate means exist to implement the policy, and
• social, cultural, and political factors.

For example, many argue that there is overwhelming evidence to support increased public policy restrictions on access to and use of cigarettes. Cigarette smoking is said to be linked to 85–90 percent of lung cancer cases. In 1998, 171,500 new cases of lung cancer were predicted. Of these, 160,100 were expected to end in death. Public policy prohibitions on cigarette use and access may be seen to satisfy four of the five criteria: (1) the cost of the policy would be minimal because cigarette access and use restrictions are in place, (2) the urgency of the situation is serious given the large number of deaths, (3) prohibiting purchase by minors and raising the prices (through taxation) are seen as effective, and (4) means are already in place for additional restrictions. The challenge in this era of high economic interest in cigarette production is the social, cultural, and political considerations (5).

Where do we spend our money? A consequence of allowing unhealthful habits, such as smoking, is that public funds may be spent on cancer treatments instead of on other societal benefits, such as improved school facilities.

It is important to recognize that sometimes the best public policy is not to enact a law in response to a controversy, but rather to allow individuals, families, communities, and societies to act in the manner they choose. Clearly, de jure public policy can only go so far in regulating people's behaviors. De jure public policy in the United States offers no match for the addictive power of nicotine and the marketing clout of the tobacco industry. In addition, any decline in cigarette use brought about by de jure public policy in the United States has been more than offset in recent years by a rapid increase of cigarette consumption elsewhere in the world.

When no laws exist to regulate behavior, public policy is called de facto (actual) public policy. With regard to lung cancer prevention programs, many think that other approaches are needed: improved general education and cultivation of an antismoking ethos. In any discussion of society's response to a social problem, it is important to think about other ways to address the problem.

Knowledge, choice, behavior, and human welfare

We can conclude that science plays an important role in assisting individuals to make choices about enhancing personal and public welfare. Science provides evidence that can be used to support ways of understanding and treating human disease, ill ness, deformity, and dysfunction. But the relationships between scientific information and human choices, and between choices and behaviors, are not linear. Human choice allows individuals to choose against sound knowledge, and choice does not necessarily lead to particular actions.

Nevertheless, it is increasingly difficult for most of us to deny the claims of science. We are continually presented with great amounts of relevant scientific and medical knowledge that is publicly accessible. We are fortunate to have available a large amount of convincing data about the development, nature, and treatment of particular cancers. As a consequence, we might be encouraged to think about the relationships among knowledge, choice, behavior, and human welfare in the following ways:

One of the goals of this module is to encourage students to think in terms of these relationships, now and as they grow older.

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The following glossary was modified from the glossary on the National Cancer Institute's Web site, available from http://www.nci.nih.gov .

Type of blood cancer that originates in lymphatic cells of the bone marrow.

Type of blood cancer that involves accumulation of myeloid cells in the bone marrow and bloodstream.

Cancer that begins in cells that line certain internal organs.

Noncancerous tumor.

Protein often found in abnormal amounts in the blood of patients with liver cancer.

Mutagenesis assay (a measure of mutagenic ability) that involves specially engineered strains of bacteria. Because of the relationship between mutagenicity and carcinogenicity, the test is used as a rapid and relatively inexpensive first screening of untested chemicals that are suspected to be carcinogens.

Term used to describe cancer cells that divide rapidly and bear little or no resemblance to normal cells.

Blood vessel formation, which usually accompanies the growth of malignant tissue.

Type of cancer that begins in the lining of blood vessels.

Normal cellular process involving a genetically programmed series of events leading to the death of a cell.

Presenting no signs or symptoms of disease.

Hereditary disorder characterized by problems with muscle coordination, immunodeficiency, inadequate DNA repair, and an increased risk of developing cancer.

Benign (noncancerous) condition in which tissue has certain abnormal features.

Small, round cell found in the lower part, or base, of the epidermis, the outer layer of the skin.

Type of skin cancer that arises from the basal cells.

Not cancerous; does not invade nearby tissue or spread to other parts of the body.

A noncancerous growth that does not spread to other parts of the body.

Use of the body's immune system, either directly or indirectly, to fight cancer or to lessen side effects that may be caused by some cancer treatments. Also known as immuno-therapy, biotherapy, or biological response modifier therapy.

Removal of a sample of tissue, which is then examined under a microscope to check for cancer cells.

Soft, spongy tissue in the center of large bones that produces white blood cells, red blood cells, and platelets.

Removal of a small sample of bone marrow (usually from the hip) through a needle for examination under a microscope to see whether cancer cells are present.

Removal of a sample of tissue from the bone marrow with a large needle. The cells are checked to see whether they are cancerous. If cancerous plasma cells are found, the pathologist estimates how much of the bone marrow is affected. Bone marrow biopsy is usually done at the same time as bone marrow aspiration.

Procedure in which doctors replace marrow destroyed by treatment with high doses of anticancer drugs or radiation. The replacement marrow may be taken from the patient before treatment or may be donated by another person.

Technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected and travels through the bloodstream. It collects in the bones, especially in abnormal areas of the bones, and is detected by a scanner.

Internal radiation therapy using an implant of radioactive material placed directly into or near the tumor.

Gene located on chromosome 17 that normally helps restrain cell growth. Inheriting an altered version of BRCA1 predisposes an individual to breast, ovarian, or prostate cancer.

Gene located on chromosome 13 that scientists believe may account for 30 to 40 percent of all inherited breast cancer.

Surgery to rebuild a breast's shape after a mastectomy.

Type of non-Hodgkin lymphoma that most often occurs in young people between the ages of 12 and 30. The disease usually causes a rapidly growing tumor in the abdomen.

Term for a group of more than 100 diseases in which abnormal cells divide without control. Cancer cells can invade nearby tissues and can spread through the bloodstream and lymphocytic system to other parts of the body.

Any substance that is known to cause cancer.

Process by which normal cells are transformed into cancer cells.

Cancer that begins in the lining or covering of an organ.

Cancer that involves only the cells in which it began and has not spread to other tissues.

Laboratory test to measure the level of carcinoembryonic antigen (CEA), a substance that is sometimes found in an increased amount in the blood of patients with certain cancers.

Sequence of events by which cells enlarge and divide. Includes stages typically named G1, S, G2, and M.

Use of natural or laboratory-made substances to prevent cancer.

Treatment with anticancer drugs.

Type of blood cancer that involves overproduction of mature lymphocytes.

Type of blood cancer that involves accumulation of granulocytes (a type of white blood cell) in the bone marrow and bloodstream.

Research study that involves patients. Each study is designed to find better ways to prevent, detect, diagnose, or treat cancer and to answer scientific questions.

Procedure that uses a flexible fiber optic endoscope to examine the internal surface of the colon along its entire length.

Treatment in which two or more chemicals are used to obtain more effective results.

X-ray procedure that uses a computer to produce a detailed picture of a cross section of the body; also called CAT or CT scan.

Inhibition of cell division in normal (noncancerous) cells when they contact a neighboring cell.

See computed tomography.

Poisonous to cells. In chemotherapy, used to describe an agent that is poisonous to cancer cells.

Process of identifying a disease by the signs and symptoms.

Abnormal cells that are not cancer.

Atypical moles; moles whose appearance is different from that of common moles. Dysplastic nevi are generally larger than ordinary moles and have irregular and indistinct borders. Their color often is not uniform and ranges from pink or even white to dark brown or black; they usually are flat, but parts may be raised above the skin surface.

Confined to a specific area; an encapsulated tumor remains in a compact form.

Having to do with the mucous membrane that lines the cavity of the uterus.

Smoke that comes from the burning end of a cigarette and smoke that is exhaled by smokers. Also called ETS or secondhand smoke. Inhaling ETS is called involuntary or passive smoking.

Study of the factors that affect the prevalence, distribution, and control of disease.

Upper or outer layer of the two main layers of cells that make up the skin.

Virus that has been associated with the development of infectious mononucleosis and also with Burkitt lymphoma.

Female hormone produced by the ovary. Responsible for secondary sex characteristics and cyclic changes in the lining of the uterus and vagina.

Study of the causes of abnormal condition or disease.

Inherited condition in which several hundred polyps develop in the colon and rectum. These polyps have a high potential to become malignant.

Test to reveal blood hidden in the feces, which may be a sign of colon cancer.

Parts of fruits and vegetables that cannot be digested. Also called bulk or roughage.

Benign uterine tumor made up of fibrous and muscular tissue.

Treatment that alters genes (the basic units of heredity found in all cells in the body). In studies of gene therapy for cancer, researchers are trying to improve the body's natural ability to fight the disease or to make the tumor more sensitive to other kinds of therapy.

Inherited; having to do with information that is passed from parents to children through DNA in the genes.

Describes how closely a cancer resembles normal tissue of its same type, along with the cancer's probable rate of growth.

System for classifying cancer cells in terms of how malignant or aggressive they appear microscopically. The grading of a tumor indicates how quickly cancer cells are likely to spread and plays a role in treatment decisions.

Member of the herpes family of viruses. One type of herpes virus is sexually transmitted and causes sores on the genitals.

Treatment of cancer by removing, blocking, or adding hormones.

Viruses that generally cause warts. Some papillomaviruses are sexually transmitted. Some of these sexually transmitted viruses cause wartlike growths on the genitals, and some are thought to cause abnormal changes in cells of the cervix.

Precancerous condition in which there is an increase in the number of normal cells lining an organ.

Tests that produce pictures of areas inside the body.

Treatment that uses the body's natural defenses to fight cancer. Also called biotherapy or biological modifier response therapy.

Number of new cases of a disease diagnosed each year.

Number of new cases per year per 100,000 persons.

Preneoplastic change in the genetic material of cells caused by a chemical carcinogen. Cancer develops when initiated cells are subsequently exposed to the same or another carcinogen.

Cancer that has remained within the tissue in which it originated.

As related to cancer, the spread of cancer cells into healthy tissue adjacent to the tumor.

Cancer that has spread beyond the layer of tissue in which it developed.

Insoluble protein that is the major constituent of the outer layer of the skin, nails, and hair.

Area of abnormal tissue change.

Cancer of the blood cells.

Probability that a person, over the course of a lifetime, will develop cancer.

Rare family predisposition to multiple cancers, caused by an alteration in the p53 tumor suppressor gene.

An enclosed space bounded by an epithelial membrane; for example, the lumen of the gut.

Cancerous; can invade nearby tissue and spread to other parts of the body.

Skin pigment (substance that gives the skin its color). Dark-skinned people have more melanin than light-skinned people.

Cell in the skin that produces and contains the pigment called melanin.

Cancer of the cells that produce pigment in the skin. Melanoma usually begins in a mole.

Cancer growth (secondary tumors) that is anatomically separated from the site at which the original cancer developed.

To spread from one part of the body to another. When cancer cells metastasize and form secondary tumors, the cells in the metastatic tumor are like those in the original (primary) tumor.

Area on the skin (usually dark in color) that contains a cluster of melanocytes. See also nevus.

Population of cells that was derived by cell division from a single ancestral cell.

Number of deaths per 100,000 persons per year.

Any substance that is known to cause mutations.

Process by which mutations occur.

Change in the way cells function or develop, caused by an inherited genetic defect or an environmental exposure. Such changes may lead to cancer.

The largest of the 24 separate institutes, centers, and divisions of the National Institutes of Health. The NCI coordinates the federal government's cancer research program.

One of eight health agencies of the Public Health Service (the Public Health Service is part of the U.S. Department of Health and Human Services). Composed of 24 separate institutes, centers, and divisions, NIH is the largest biomedical research facility in the world.

Cell death.

Abnormal new growth of cells.

New growth of tissue. Can be referred to as benign or malignant.

Medical term for a spot on the skin, such as a mole. A mole is a cluster of melanocytes that usually appears as a dark spot on the skin.

One of the several types of lymphoma (cancer that develops in the lymphocytic system) that are not Hodgkin lymphoma. Hodgkin lymphoma is rare and occurs most often in people aged 15 to 34 and in people over 55. All other lymphomas are grouped together and called non-Hodgkin lymphoma.

Skin cancer that does not involve melanocytes. Basal cell cancer and squamous cell cancer are nonmelanoma skin cancers.

The Office of Science Education of the National Institutes of Health (NIH) coordinates science education activities at NIH and sponsors science education projects in-house.

Gene that normally directs cell growth but also can promote or allow the uncontrolled growth of cancer if damaged (mutated) by an environmental exposure to carcinogens or if damaged or missing because of an inherited defect.

Having the capacity to cause cancer.

Doctor who specializes in treating cancer. Some oncologists specialize in a particular type of cancer treatment. For example, a radiation oncologist specializes in treating cancer with radiation.

Study of tumors encompassing their physical, chemical, and biologic properties.

Surgical removal of one or both ovaries.

Gene that normally inhibits the growth of tumors, which can prevent or slow the spread of cancer.

Treatment that does not alter the course of a disease, but improves the quality of life.

Population of cells that was derived by cell division from more than one ancestral cell.

Mass of tissue that projects into the colon.

Term used to describe a condition that may or is likely to become cancer.

Growths in the colon that often become cancerous.

Female hormone produced by the ovaries and placenta; responsible for preparing the uterine lining for implantation of an early embryo.

Probable outcome or course of a disease; the chance of recovery.

Expression of the cancerous potential of initiated cells after exposure to the same or a different carcinogen.

Treatment administered or taken to prevent disease.

Gene that, when converted to an oncogene by a mutation or other change, can cause a normal cell to become malignant. Normal oncogenes function to control normal cell growth and differentiation.

Treatment with high-energy rays (such as X-rays) to kill cancer cells. The radiation may come from outside the body (external radiation) or from radioactive materials placed directly in the tumor (implant radiation). Also called radiotherapy.

Giving off radiation.

Radioactive gas that is released by uranium, a substance found in soil and rock. When too much radon is breathed in, it can damage lung cells and lead to lung cancer.

Comparison of the risk of developing cancer in persons with a certain type of exposure or characteristic with the risk in persons who do not have this exposure or characteristic.

Disappearance of the signs and symptoms of cancer. When this happens, the disease is said to be "in remission." A remission can be temporary or permanent.

Eye cancer caused by the loss of both copies of the tumor suppressor gene RB ; the inherited form typically occurs in childhood because one gene is missing from the time of birth.

Small RNA virus that has an RNA genome. Acts as a template for the production of the DNA that is integrated into the DNA of the host cell. Many retroviruses are believed to be oncogenic.

Something that increases the chance of developing a disease.

Chicken retrovirus that was the first virus shown to cause a malignancy.

Malignant tumor that begins in connective and supportive tissue.

Checking for disease when there are no symptoms.

Metastasis.

Surveillance, Epidemiology, and End Results Program of the National Cancer Institute. Started in 1973, SEER collects cancer incidence data in nine geographic areas with a combined population of approximately 9.6 percent of the total population of the United States.

Problem that occurs when treatment affects healthy cells. Common side effects of cancer treatment are fatigue, nausea, vomiting, decreased blood cell counts, hair loss, and mouth sores.

Any of the body cells except the reproductive cells.

Scale for rating sun-screens. Sunscreens with an SPF of 15 or higher provide the best protection from the sun's harmful rays.

Type of skin cancer that arises from the squamous cells.

Extent of a cancer, especially whether the disease has spread from the original site to other parts of the body.

Doing exams and tests to learn the extent of the cancer, especially whether it has spread from its original site to other parts of the body.

Cells from which all blood cells develop.

Substance that blocks the effect of the sun's harmful rays. Using lotions or creams that contain sunscreens can protect the skin from damage that may lead to cancer. See also SPF.

Proportion of patients alive at some point after their diagnosis of a disease.

Enzyme that is present and active in cells that can divide without apparent limit (for example, cancer cells and cells of the germ line). Telomerase replaces the missing repeated sequences of each telomere.

End of a chromosome. In vertebrate cells, each telomere consists of thousands of copies of the same DNA sequence, repeated again and again. Telomeres become shorter each time a cell divides; when one or more telomeres reaches a minimum length, cell division stops. This mechanism limits the number of times a cell can divide.

Male sex hormone.

Change that a normal cell undergoes as it becomes malignant.

Abnormal mass of tissue that results from excessive cell division. Tumors perform no useful body function. They may be either benign (not cancerous) or malignant (cancerous).

Substance in blood or other body fluids that may suggest that a person has cancer.

Gene in the body that can suppress or block the development of cancer.

Invisible rays that are part of the energy that comes from the sun. UV radiation can burn the skin and cause melanoma and other types of skin cancer. UV radiation that reaches the earth's surface is made up of two types of rays, UVA and UVB rays. UVB rays are more likely than UVA rays to cause sunburn, but UVA rays pass further into the skin. Scientists have long thought that UVB radiation can cause melanoma and other types of skin cancer. They now think that UVA radiation also may add to skin damage that can lead to cancer. For this reason, skin specialists recommend that people use sunscreens that block or absorb both kinds of UV radiation.

Process by which one of the two X chromosomes in each cell from a female mammal becomes condensed and inactive. This process assures that most genes on the X chromosome are expressed to the same extent in both males and females.

High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer.

Hereditary disease characterized by extreme sensitivity to the sun and a tendency to develop skin cancers. Caused by inadequate DNA repair.

• Cite this Page National Institutes of Health (US); Biological Sciences Curriculum Study. NIH Curriculum Supplement Series [Internet]. Bethesda (MD): National Institutes of Health (US); 2007. Understanding Cancer.

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Francis Collins: Why I’m going public with my prostate cancer diagnosis

I served medical research. now it’s serving me. and i don’t want to waste time..

Over my 40 years as a physician-scientist, I’ve had the privilege of advising many patients facing serious medical diagnoses. I’ve seen them go through the excruciating experience of waiting for the results of a critical blood test, biopsy or scan that could dramatically affect their future hopes and dreams.

But this time, I was the one lying in the PET scanner as it searched for possible evidence of spread of my aggressive prostate cancer . I spent those 30 minutes in quiet prayer. If that cancer had already spread to my lymph nodes, bones, lungs or brain, it could still be treated — but it would no longer be curable.

Why am I going public about this cancer that many men are uncomfortable talking about? Because I want to lift the veil and share lifesaving information, and I want all men to benefit from the medical research to which I’ve devoted my career and that is now guiding my care.

Five years before that fateful PET scan, my doctor had noted a slow rise in my PSA, the blood test for prostate-specific antigen. To contribute to knowledge and receive expert care, I enrolled in a clinical trial at the National Institutes of Health, the agency I led from 2009 through late 2021.

At first, there wasn’t much to worry about — targeted biopsies identified a slow-growing grade of prostate cancer that doesn’t require treatment and can be tracked via regular checkups, referred to as “active surveillance.” This initial diagnosis was not particularly surprising. Prostate cancer is the most commonly diagnosed cancer in men in the United States, and about 40 percent of men over age 65 — I’m 73 — have low-grade prostate cancer . Many of them never know it, and very few of them develop advanced disease.

Why am I going public about this cancer that many men are uncomfortable talking about? Because I want to lift the veil and share lifesaving information.

But in my case, things took a turn about a month ago when my PSA rose sharply to 22 — normal at my age is less than 5. An MRI scan showed that the tumor had significantly enlarged and might have even breached the capsule that surrounds the prostate, posing a significant risk that the cancer cells might have spread to other parts of the body.

New biopsies taken from the mass showed transformation into a much more aggressive cancer. When I heard the diagnosis was now a 9 on a cancer-grading scale that goes only to 10, I knew that everything had changed.

Thus, that PET scan, which was ordered to determine if the cancer had spread beyond the prostate, carried high significance. Would a cure still be possible, or would it be time to get my affairs in order? A few hours later, when my doctors showed me the scan results, I felt a rush of profound relief and gratitude. There was no detectable evidence of cancer outside of the primary tumor.

Later this month, I will undergo a radical prostatectomy — a procedure that will remove my entire prostate gland. This will be part of the same NIH research protocol — I want as much information as possible to be learned from my case, to help others in the future.

While there are no guarantees, my doctors believe I have a high likelihood of being cured by the surgery.

My situation is far better than my father’s when he was diagnosed with prostate cancer four decades ago. He was about the same age that I am now, but it wasn’t possible back then to assess how advanced the cancer might be. He was treated with a hormonal therapy that might not have been necessary and had a significant negative impact on his quality of life.

Because of research supported by NIH, along with highly effective collaborations with the private sector, prostate cancer can now be treated with individualized precision and improved outcomes.

As in my case, high-resolution MRI scans can now be used to delineate the precise location of a tumor. When combined with real-time ultrasound, this allows pinpoint targeting of the prostate biopsies. My surgeon will be assisted by a sophisticated robot named for Leonardo da Vinci that employs a less invasive surgical approach than previous techniques, requiring just a few small incisions.

Advances in clinical treatments have been informed by large-scale, rigorously designed trials that have assessed the risks and benefits and were possible because of the willingness of cancer patients to enroll in such trials.

I feel compelled to tell this story openly. I hope it helps someone. I don’t want to waste time.

If my cancer recurs, the DNA analysis that has been carried out on my tumor will guide the precise choice of therapies. As a researcher who had the privilege of leading the Human Genome Project , it is truly gratifying to see how these advances in genomics have transformed the diagnosis and treatment of cancer.

I want all men to have the same opportunity that I did. Prostate cancer is still the No. 2 killer of men. I want the goals of the Cancer Moonshot to be met — to end cancer as we know it. Early detection really matters, and when combined with active surveillance can identify the risky cancers like mine, and leave the rest alone. The five-year relative survival rate for prostate cancer is 97 percent, according to the American Cancer Society , but it’s only 34 percent if the cancer has spread to distant areas of the body.

But lack of information and confusion about the best approach to prostate cancer screening have impeded progress. Currently, the U.S. Preventive Services Task Force recommends that all men age 55 to 69 discuss PSA screening with their primary-care physician, but it recommends against starting PSA screening after age 70.

Other groups, like the American Urological Association , suggest that screening should start earlier, especially for men with a family history — like me — and for African American men, who have a higher risk of prostate cancer. But these recommendations are not consistently being followed.

Our health-care system is afflicted with health inequities. For example, the image-guided biopsies are not available everywhere and to everyone. Finally, many men are fearful of the surgical approach to prostate cancer because of the risk of incontinence and impotence, but advances in surgical techniques have made those outcomes considerably less troublesome than in the past. Similarly, the alternative therapeutic approaches of radiation and hormonal therapy have seen significant advances.

A little over a year ago, while I was praying for a dying friend, I had the experience of receiving a clear and unmistakable message. This has almost never happened to me. It was just this: “Don’t waste your time, you may not have much left.” Gulp.

Having now received a diagnosis of aggressive prostate cancer and feeling grateful for all the ways I have benefited from research advances, I feel compelled to tell this story openly. I hope it helps someone. I don’t want to waste time.

Francis S. Collins served as director of the National Institutes of Health from 2009 to 2021 and as director of the National Human Genome Research Institute at NIH from 1993 to 2008. He is a physician-geneticist and leads a White House initiative to eliminate hepatitis C in the United States, while also continuing to pursue his research interests as a distinguished NIH investigator.

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• Francis Collins: Why I’m going public with my prostate cancer diagnosis April 12, 2024 Francis Collins: Why I’m going public with my prostate cancer diagnosis April 12, 2024