# data[].attributes.body
http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1349-7006

Library Database

Instagram

Twitter

Links that are connected to the sticky notes

# data[].attributes.attachment_link.title
Chromosome 13: BRCA2 gene for breast cancer susceptibility, Matt Ridley :: DNA Learning Center

# data[].attributes.attachment_link.description
Interviewee: Matt Ridley. BRCA2, on chromosome 13, is one of the genes associated with hereditary breast cancer. Although gender, age and environmental effects are major risk factors for breast cancer, having a mutation in either the BRCA2 gene or BRCA1 gene (on chromosome 17) increases the risk.

# data[].attributes.attachment_link.readable_text
That's bad luck -- and it's the primary cause of most cancer cases, says a Johns Hopkins Medicine research study.

Roughly two-thirds of cancers in adults can be attributed to random mutations in genes capable of driving cancer growth, said two scientists who ran statistics on cancer cases.

That may sound jaw-dropping. And Johns Hopkins anticipates that the study will change the way people think about cancer risk factors.

They also believe it could lead to changes in the funding of cancer studies, with a greater focus on finding ways to detect those cancers attributed to random mutations in genes at early, curable stages.
Smoking can still kill you
But, no, that's not permission to smoke or to not use sunblock.

Some forms of cancer are exceptions, where lifestyle and environment play a big role. Lung cancer is one of them. So is skin cancer.

And, if cancer runs in your family, this unfortunately doesn't mean you're in the clear. Some cancers are more strongly influenced by genetic heritage than others.

"The remaining third (of cancer cases) are due to environmental factors and inherited genes," the Kimmel Cancer Center said in a statement on the study published Friday in the magazine Science.

In fact, all three factors work together.

"All cancers are caused by a combination of bad luck, the environment and heredity, and we've created a model that may help quantify how much of these three factors contribute to cancer development," said cancer researcher Bert Vogelstein.

An unhealthy lifestyle can compound matters, but more for some cancers than for others, the scientists said.

"Changing our lifestyle and habits will be a huge help in preventing certain cancers, but this may not be as effective for a variety of others," medical statistician Cristian Tomasetti said.

He placed heavy emphasis on early detection.

Stem cells in our organs divide constantly to replenish damaged tissue. Sometimes there are random mistakes in the replication of DNA, small mutations, Vogelstein said.

Some genes, when they mutate, are more apt to promote cancer growth.

"The more these mutations accumulate, the higher the risk that cells will grow unchecked, a hallmark of cancer," Vogelstein said.

Scientist have known this for a long time, but what the study reveals was how big of an influence it is.

"The actual contribution of these random mistakes to cancer incidence, in comparison to the contribution of hereditary or environmental factors, was not previously known," says Vogelstein.

Dr. Otis Brawley, chief medical officer for the American Cancer Society, told CNN the study was "good science" that backed up what many scientists already thought.

"This is actually just confirmation of something that we have known for probably 20 years," he said.

"As we have learned more and more about cancer ... we've come to realize that a number of cancers start purely because of mutations that happen that are just unexplainable. Bad luck is, unfortunately, the right way to explain it."

Those cancers that develop have escaped at least three fail-safe systems in the body that deal with these cell mutations, he said; these are programmed cell death, or apoptosis, DNA repair enzymes and certain cells in the immune system.
Cell division and statistics
For their study, the two scientists came up with an average total number of cell divisions in 31 different tissues within a human lifetime. And they looked at the cancer risk in each of those tissues.

They determined that the more a tissue's cells divide, the higher the chance cancer could develop in that tissue.

"Our study shows, in general, that a change in the number of stem cell divisions in a tissue type is highly correlated with a change in the incidence of cancer in that same tissue," says Vogelstein.

Colon tissue, for example, divides much more than other intestinal tissue, and cancer in the colon is much more prevalent there, the study said.

With colon tissue, the scientists took environmental influences into account.

Doing the math overall, the two scientists arrived at a rate at which cancer risk can be explained by the cell divisions. It was 65%, they said.

But the researchers drew a line between one group of cancers and another. Of the 31 they looked at, they determined that 22 were basically "bad luck" cancers.

But nine others appeared at rates noticeably higher than could be expected from cell division alone -- which the researchers said is probably due to habits, pollution or genetics.

No surprise: Lung cancer and skin cancer were two of them, they said. Smoking and too much sun exposure are still strongly linked to those cancers.

Brawley said the study's findings should be no reason to alter behaviors shown to lessen the risk of cancer.

"We have good epidemiological data to show that people can reduce their risk of cancer and I would encourage them to do those things," he said.

They include not smoking, managing their weight so they don't become obese and taking physical exercise, he said.

As for the suggestion the study's findings may prompt changes in funding, Brawley said he would be pleased just to see more money go into research.

"Only 10% of the grants submitted to the NIH (National Institutes of Health) actually get funded because we have such a shortage of money," he said.

"We invested in the United States last year $5 billion in cancer research. I would like to see more."

CNN's Laura Smith-Spark and Alexander Felton contributed to this report.

# data[].attributes.attachment_link.keywords[]
cancer: 'bad luck' seen as primary cause in study - cnn

# data[].attributes.attachment_link.title
Cancer: 'Bad luck' seen as primary cause in study - CNN

# data[].attributes.attachment_link.description
That's bad luck -- and it's the primary cause of most cancer cases, says a Johns Hopkins Medicine research study. Roughly two-thirds of cancers in adults can be attributed to random mutations in genes capable of driving cancer growth, said two scientists who ran statistics on cancer cases. That may sound jaw-dropping.

# data[].attributes.attachment_link.description
This page answers questions like, is cancer genetic? Can cancer run in families? How do genetic changes cause cancer? Should I get genetic testing for cancer risk?

# data[].attributes.headline
How Scientists Are Dealing With Mutations

# data[].attributes.subject
How Scientists Are Dealing With Mutations

# data[].attributes.attachment_link.readable_text
In normal cells, hundreds of genes intricately control the process of cell division. Normal growth requires a balance between the activity of those genes that promote cell proliferation and those that suppress it. It also relies on the activities of genes that signal when damaged cells should undergo apoptosis.

Cells become cancerous after mutations accumulate in the various genes that control cell proliferation. According to research findings from the Cancer Genome Project, most cancer cells possess 60 or more mutations. The challenge for medical researchers is to identify which of these mutations are responsible for particular kinds of cancer. This process is akin to searching for the proverbial needle in a haystack, because many of the mutations present in these cells have little to nothing to do with cancer growth.

Different kinds of cancers have different mutational signatures. However, scientific comparison of multiple tumor types has revealed that certain genes are mutated in cancer cells more often than others. For instance, growth-promoting genes, such as the gene for the signaling protein Ras, are among those most commonly mutated in cancer cells, becoming super-active and producing cells that are too strongly stimulated by growth receptors. Some chemotherapy drugs work to counteract these mutations by blocking the action of growth-signaling proteins. The breast cancer drug Herceptin, for example, blocks overactive receptor tyrosine kinases (RTKs), and the drug Gleevec blocks a mutant signaling kinase associated with chronic myelogenous leukemia.

Other cancer-related mutations inactivate the genes that suppress cell proliferation or those that signal the need for apoptosis. These genes, known as tumor suppressor genes, normally function like brakes on proliferation, and both copies within a cell must be mutated in order for uncontrolled division to occur. For example, many cancer cells carry two mutant copies of the gene that codes for p53, a multifunctional protein that normally senses DNA damage and acts as a transcription factor for checkpoint control genes.

# data[].attributes.attachment_link.description
In normal cells, hundreds of genes intricately control the process of cell division. Normal growth requires a balance between the activity of those genes that promote cell proliferation and those that suppress it. It also relies on the activities of genes that signal when damaged cells should undergo apoptosis.

# data[].attributes.body
the simulation of growth of a small tumor. Different colors correspond to cells with different driver mutations, and this is the tumour at its biggest point.

# data[].attributes.attachment_link.readable_text
Videos reveal the growth, mutation and evolution of a lethal cancer

shed new light on how cancers develop resistance to drugs and chemotherapy.

They look almost like a piece of modern art, but these groundbreaking three-dimensional computer models actually show a solid tumour grows.

They incredible videos reveal the growth, mutation and evolution of lethal tumours.

Scientists say it will help them to understand how lethal cancers develop resistance to drugs and chemotherapy.

The collaboration between Harvard, Edinburgh, and Johns Hopkins Universities including Martin Nowak, Director of the Program for Evolutionary Dynamics and Professor of Mathematics and of Biology at Harvard, has now developed the first model of solid tumors that reflects both their three-dimensional shape and genetic evolution.

'Previously, we and others have mostly used non-spatial models to study cancer evolution,' Nowak said.

'But those models do not describe the spatial characteristics of solid tumors.

'Now, for the first time, we have a computational model that can do that.'

A key insight of the new model, Nowak said, is the ability for cells to migrate locally.

'Cellular mobility makes cancers grow fast, and it makes cancers homogenous in the sense that cancer cells share a common set of mutations.

'It is responsible for the rapid evolution of drug resistance,' Nowak said.

'I further believe that the ability to form metastases, which is what actually kills patients, is a consequence of selection for local migration.'

The new model explains why cancer cells have a surprising number of genetic mutations in common, how driver mutations spread through the whole tumor and how drug resistance evolves.

The study is described in an August 26 paper in Nature.

Nowak and colleagues, including Bartek Waclaw of the University of Edinburgh, who is the first author of the study, Ivana Bozic of Harvard University and Bert Vogelstein of Johns Hopkins University, set out to improve on past models, because they were unable to answer critical questions about the spatial architecture of genetic evolution.

In the videos, similar colours denote similar mutations and - as the tumour grows - they remain clustered together, as also shown by experiment.

Of the billions of cancer cells that exist in a patient, only a tiny percentage - about one in a million - are resistant to drugs used in targeted therapy.

When treatment starts, the video shows how non-resistant cells are wiped out - but the few resistant cells quickly repopulate the cancer.

'The majority of the mathematical models in the past counted the number of cells that have particular mutations, but not their spatial arrangement,' Nowak said.

Understanding that spatial structure is important, he said, because it plays a key role in how tumors grow and evolve.

In a spatial model cells divide only if they have the space to do so.

This results in slow growth unless cells can migrate locally.

'By giving cells the ability to migrate locally,' Nowak said, 'individual cells can always find new space where they can divide.

The result isn't just faster tumor growth, but a model that helps to explain why cancer cells share an unusually high number of genetic mutations, and how drug resistance can rapidly evolve in tumors.

As they divide, all cells - both healthy and cancerous - accumulate mutations, Nowak said, and most are so called 'passenger' mutations that have little effect on the cell.

In cancer cells, however, approximately 5 percent are what scientists call 'driver' mutations - changes that allow cells to divide faster or live longer.

In addition to rapid tumor growth, those mutations carry some previous passenger mutations forward, and as a result cancer cells often have a surprising number of mutations in common.

Similarly, drug resistance emerges when cells mutate to become resistant to a particular treatment.

While targeted therapies wipe out nearly all other cells, the few resistant cells begin to quickly replicate, causing a relapse of the cancer.

'This migration ability helps to explain how driver mutations are able to dominate a tumor, and also why targeted therapies fail within a few months as resistance evolves,' Nowak said. 'So what we have is a computer model for solid tumors, and it's this local migration that is of crucial importance.'

'Our approach does not provide a miraculous cure for cancer.' said Bartek Waclaw, 'However, it suggests possible ways of improving cancer therapy.

One of them could be targeting cellular motility (that is local migration) and not just growth as standard therapies do.'

# data[].attributes.attachment_link.title
The beauty of CANCER: Researchers reveal 3D models of tumours

# data[].attributes.attachment_link.description
Videos reveal the growth, mutation and evolution of a lethal cancer shed new light on how cancers develop resistance to drugs and chemotherapy. They look almost like a piece of modern art, but these groundbreaking three-dimensional computer models actually show a solid tumour grows. They incredible videos reveal the growth, mutation and evolution of lethal tumours.

# data[].attributes.body
This post explains to its followers how cancer is caused by a mutation.

# data[].attributes.headline
Instagram Account That Teaches About Cancer.

# data[].attributes.subject
Instagram Account That Teaches About Cancer.

# data[].attributes.attachment_link.title
All about cancer (@cancer_science) * Instagram photos and videos

# data[].attributes.attachment_link.description
32 Followers, 1 Following, 18 Posts - See Instagram photos and videos from All about cancer (@cancer_science)

# data[].attributes.body
An account on Instagram informing followers about the science behind cancer

# data[].attributes.body
"A new, faster way to identify cancer-causing mutations in the DNA of tumor cells may pave the way for the next generation of
custom-tailored cancer therapies''

# data[].attributes.attachment_link.readable_text
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

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 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.

When Cancer Spreads

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.

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:

Carcinoma

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.

Sarcoma

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.

Leukemia

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

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

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.

# data[].attributes.attachment_link.description
Explanations about what cancer is, how cancer cells differ from normal cells, and genetic changes that cause cancer to grow and spread.

# data[].attributes.attachment_link.readable_text
Improving the lives of all people through cancer research

NCI is the nation's trusted source for cancer information. We are here for you with information about causes and risk factors, symptoms, how cancer is diagnosed, and treatment options.

Support for the best science underpins everything NCI does. Explore our resources to help researchers conduct their work and apply for funding and training opportunities.

Featured News and Research

Bringing Data to Life for Cancer Research

# data[].attributes.attachment_link.description
Accurate, up-to-date, comprehensive cancer information from the U.S. government's principal agency for cancer research.

# data[].attributes.attachment_link.title
Florida Teen Initially Diagnosed with the Flu Discovers He Actually Has Stage 4 Cancer

# data[].attributes.attachment_link.description
"Hearing from people that I'm an inspiration has made me feel better than I ever could have imagined," Hunter Brady tells PEOPLE

# data[].attributes.body
All cancers begin when one or more genes in a cell are mutated, or changed. This creates an abnormal protein or no protein at all. An abnormal protein provides different information than a normal protein, which can cause cells to multiply uncontrollably and become cancerous.

# data[].attributes.body
Genes control how your cells work by making proteins that have specific functions and act as messengers for the cell. Therefore, each gene must have the correct instructions or "code" for making its protein. This is so the protein can perform the correct function for the cell.

# data[].attributes.body
Genes are located on 46 chromosomes, which are arranged in two sets of 23 chromosomes. You inherit one set of chromosomes from your mother and one set from your father. One chromosome in each set of 23 determines whether you are female or male. The other 22 chromosome pairs, called autosomes, determine your other physical characteristics.

# data[].attributes.body
Genes are found in the DNA in each cell that makes up your body. They control how the cell functions, including how quickly it grows, how often it divides, and how long it lives. Researchers estimate that there are 30,000 different genes in each cell.