A Single Cell Shines New Light on How Cancers Develop

A Single Cell Shines New Light on How Cancers Develop
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Posted by:
Greg Lance – Watkins
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A Single Cell Shines New Light on How Cancers Develop

By GINA KOLATAJAN. 28, 2016

Zebra fish in the lab of Dr. Leonard Zon. The tiny transparent creatures allow researchers to see cells and organs without cutting the fish open. Credit Shiho Fukada for The New York Times

It was just a tiny speck, a single cell that researchers had marked with a fluorescent green dye. But it was the very first cell of what would grow to be a melanoma, the deadliest form of skin cancer. Never before had researchers captured a cancer so early.

The cell was not a cancer yet. But its state was surprising: It was a cell that had reverted to an embryonic form, when it could have developed into any cell type. As it began to divide, cancer genes took over and the single primitive cell barreled forward into a massive tumor.

Those were the findings of Dr. Leonard Zon of Boston Children’s Hospital, Dr. Charles K. Kaufman, and their colleagues, in a study published Thursday in the journal Science that offers new insight into how cancers may develop. The researchers stumbled on that first cell of a melanoma when they set out to solve a puzzle that has baffled cancer investigators: Why do many cells that have cancer genes never turn cancerous?

The work was in fish that had been given human genes, but the investigators found the same genetic programs in human melanomas, indicating that they too started when a cell reverted to an embryonic state. Much more study is needed, but researchers say the result can help them understand why melanomas and possibly other cancers form, and potentially prevent them. And it may provide a way to stop melanomas from growing back after they have been cut down by new targeted drugs.

Dr. Leonard I. Zon, at of Boston Children’s Hospital, poses for a portrait with an aquarium of zebra fish at the Karp Family Research Building in Boston, MA. Credit Shiho Fukada for The New York Times
“It’s a significant advance in the field,” said Ze’ev Ronai, the scientific director of La Jolla Sanford Burnham Prebys Medical Discovery Institute, a nonprofit research center. Dr. Ronai was not involved in the study.

The prevailing idea about the development of a cancer is that genes randomly mutate in a healthy cell, perhaps from sun exposure, perhaps from simple bad luck. The mutated genes drive aberrant cell growth, and the growing mass of cells accumulates more and more mutations that drive it to grow faster and spread until, finally, a cancer is formed.

Yet researchers keep finding cancer genes in perfectly normal, healthy cells that never turn malignant. These are genes that take the brakes off cell growth and are considered essential drivers of tumor growth.

Human skin cells are exemplars of the effect. In one study, Peter Campbell and his colleagues at Cambridge University looked for 74 cancer genes in normal skin cells. In many they saw the same pattern of mutations as is found in skin cancers. But since these cells were not cancerous, they realized something must be missing. What, besides powerful cancer genes, is needed to make a cancer?

Moles also show the effect. “One of the things we’ve known about moles is that the vast majority never will become melanomas,” said Dr. Keith T. Flaherty, a melanoma expert at Massachusetts General Hospital who was not associated with the new study. “The odds are against it.” Yet almost every mole contains one of two potent gene mutations that are characteristic of melanomas, BRAF or NRAS, he added, and a third also harbor another notorious cancer gene, P53. New targeted drugs that block BRAF can slow melanoma growth.

 

“More and more data suggest that just having mutations is not sufficient to cause cancer,” said Dr. Kornelia Polyak, a breast cancer researcher at the Dana-Farber Cancer Institute, who was not associated with the new study. “You need the right context.”

That was where Dr. Zon and his colleagues began 10 years ago. They were investigating melanoma by creating it in zebra fish, tiny transparent creatures that allow researchers to see cells and organs without cutting the fish open. The researchers put human BRAF and P53 genes in every melanocyte, the pigmented skin cells, of the fish. If genes were all that was needed for cancer, the fish would explode with melanoma. But the researchers found only one to three melanomas per fish.

“That told us there has to be an additional event,” Dr. Zon said.

By luck, they found it. The pigmented skin cells that became cancerous had turned on a gene, crestin, that is normally activated only in cells that are part of the neural crest, a group of cells pinched off early in embryonic life from a region adjacent to the brain. These primitive cells, depending on where they are in the embryo, can turn into pigmented skin cells or a variety of other types of cells, like those that make up bones and teeth, the covering of the brain or those that sheath and insulate nerve cells. Once cells develop into their mature tissue type — pigmented skin cell, bone or tooth, for example — the crestin gene shuts down. Those pigmented skin cells in the fish that had an active crestin gene had reverted to that primitive state when they were malleable, their fates still wide open.

The investigators marked cells with an active crestin gene with a fluorescent dye, enabling them to spot the cells because they glowed bright green. Then they observed what happened. Every time a cell lit up green it divided and turned into a cancer. Cells that did not light up never turned into a cancer.

That makes sense, Dr. Polyak said, because such primitive cells are more proliferative and more able to spread throughout the body. That is their role during development. They also can develop their own blood supply, something tumors do, too.

The zebra fish work was convincing, Dr. Ronai said. “They provide a pretty strong demonstration that that pathway is correct,” he said. “It’s a significant advance in the field.” It can, he said, allow researchers to monitor the early development of melanomas.

But it also gives rise to a host of questions and hypotheses. These include why melanomas with BRAF mutations eventually become resistant to drugs that block the BRAF cancer gene. Could it be, Dr. Flaherty suggests, that the drugs prune off only the melanoma cells that grew from the original embryo-like seed cell? Might the drugs be sparing the embryo-like seed cell, freeing it to form another cancer? If so, those seed cells could be a new drug target. The hope is that if they are destroyed, the tumor will be gone for good.

But, Dr. Polyak asked, why then would a pigmented skin cell spontaneously revert to a primitive embryo cell? “What is the stimulus that allows a single cell out of millions to become cancerous?” she said. “Why does it turn on, this particular genetic program? What is the trigger and why does it happen so rarely? Why, why is this happening?”

With the zebra fish model, Dr. Zon says, “we have the ability to ask.”

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A Grim Breast Cancer Milestone for Black Women

Posted by: Greg Lance – Watkins
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A Grim Breast Cancer Milestone for Black Women
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I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
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I just want to say sorry for copping out at times and leaving my wife Lee and friends to cope!
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I do make a lousy patient!

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Hi,

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A Grim Breast Cancer Milestone
for Black Women

By TARA PARKER-POPE OCTOBER 29, 2015 10:00 AM October 29, 2015 10:00 am 20 Comments
Debrah Reid, 59, center, in 2013, relaxed with her sister, Audrey Anderson, left, and friend Travia Davis, at her home in Memphis. Ms. Reid was given a breast cancer diagnosis in 2013 and was featured in an article on racial disparities in breast cancer that year. Ms. Reid died in May 2015 from the disease.
Debrah Reid, 59, center, in 2013, relaxed with her sister, Audrey Anderson, left, and friend Travia Davis, at her home in Memphis. Ms. Reid was given a breast cancer diagnosis in 2013 and was featured in an article on racial disparities in breast cancer that year. Ms. Reid died in May 2015 from the disease.
Credit Ruth Fremson/The New York Times

African-American women in the United States have reached a dubious milestone. For the first time, the incidence of breast cancer among black women is equal to that of white women, according to a sweeping new report from the American Cancer Society.

The finding is worrisome because breast cancer has historically been more deadly in black women than in white women, but at least it has not been as common. Now, as incidence rates equalize, the data suggest that breast cancer will continue to exact a far greater toll on black women, and that the trend shows no sign of abating.

“It’s been known that white women are more likely to be diagnosed with breast cancer, but black women are more likely to die from it,” said Carol E. DeSantis, senior epidemiologist at the American Cancer Society and the lead author of the report. “Now what happens? Now the incidence rates are similar, and black women are still more likely to die from it. Our conclusion is that the widening mortality disparity is likely to continue, especially now in light of the increasing incidence.”

The data were obtained from the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute, a program that has been collecting information on cancer patients since 1973.

Among white women breast cancer incidence rates have been stable since 2004, hovering around 135 per 100,000 women. But among black women, rates have been consistently lower, ranging from 119 to 125 per 100,000. But in 2012, a startling change occurred. The incidence rate moved to 135 cases per 100,000 women for both white and black women.

“The lines have crossed for the first time,” Ms. DeSantis said. “There is variation in year-to-year rates, especially in smaller populations such as in black women, but I think, overall, the picture we’ve seen is this slow steady increase in black women and stable rates in white women.”

While it’s possible that a fraction of the rise could be attributed to earlier detection, that would not fully explain the trend because rates at which women are being screened for breast cancer have remained stable. As a result, the trends suggest that the uptick in incidence is not a result of doctors simply finding more cases of breast cancer, but is probably the result of other factors.

“To me the bottom line of these statistics is the evidence that the health disparity between African-American and white women in the U.S. is still going strong,” said Kirsten Moysich, a professor of oncology at the Roswell Park Cancer Institute in Buffalo, N.Y. “And it’s even more pronounced than previously reported.”

Researchers say the reasons behind the increase are likely to be complex, but rising obesity rates among African-American women may explain some of it. Obesity has been linked to an increased risk of estrogen-receptor positive breast cancers, and much of the increase in breast cancers among black women has been due largely to more cases of this type of tumor. The obesity rate in black women was 58 percent during the 2009 to 2012 period, up from 39 percent from 1999 to 2002. Meanwhile, the obesity rate among white women has stabilized at around 33 percent.

Researchers also believe that changes in reproductive patterns may play a role, as more African-American women delay childbirth and have fewer children. Both are recognized risk factors for breast cancer.

Over all, the report painted a grim picture of the state of breast cancer in African-American women, showing that advances in diagnosis and treatment that have dramatically improved survival rates from breast cancer and saved countless lives have largely bypassed African-American women. By virtually every measure of the disease — age of diagnosis, age of death, stage of diagnosis — black women are at a significant disadvantage compared with white women, the data show.

Black women are given breast cancer diagnoses at younger ages and die from the disease at younger ages than white women, suggesting that the disease may exact a greater economic and family toll on the black community by stealing more of a woman’s most productive years. The median age at diagnosis is 58 for black women and 62 for white women. The median age for breast cancer death is 62 for black women and 68 for white women.

Black women also are less likely than white women are to be given a diagnosis of early stage disease, and more likely to be given a diagnosis with later stage, and less treatable, tumors, according to the report.

Compared with white women, black women were more likely to be found to have an aggressive form of the disease called triple negative breast cancer, which has a poorer prognosis, in part, because there are not targeted therapies to treat it. Triple negative breast cancers account for 22 percent of the cases among black women, and 11 percent among white women.

Black women also lag behind white women in diagnosis of estrogen-receptor positive disease, the most treatable form of breast cancer. Among white women, 76 percent of cancers diagnosed are ER positive, compared with 62 percent in black women.

Over all, a black woman given a breast cancer diagnosis is 42 percent more likely to die from the disease than a white woman with breast cancer. An analysis of breast cancer mortality trends in 41 of the largest cities in the United States, published last year in Cancer Epidemiology, found that in some cities the risk is even greater. In Los Angeles, a black woman with breast cancer is about 70 percent more likely to die from the disease than a white woman is. In Memphis, black women face more than double the risk.

Researchers say the racial divide in breast cancer mortality may be due to a combination of factors, including disparities in the quality of care available to black women, who may have less access to quality screening and treatment, compared to white women. Lower rates of follow-up after a mammogram, cultural distrust of doctors, and lack of insurance coverage among black women may also play a role.

Dr. Moysich said she hopes the data will galvanize the African-American community and the medical community in general to push for more research.

“There are a lot of people really trying to figure this out on an epidemiological basis and molecular basis and behavioral basis, but we haven’t put our finger on it,’’ she said. “There are lots of partial explanations, and this is a question a lot of people are working on, but it still confuses us.”

To view the original of this article CLICK HERE

TIMES DOCUMENTARIES By Stephen Maing 11:51
The Cancer Divide: Mary
Video: http://vp.nyt.com/video/2013/12/22/25112_1_breast-cancer-memphis_wg_720p.mp4
The Cancer Divide: Mary
Mary Singleton, 57, learned in July that she had Stage 4 breast cancer. After the diagnosis her son, George, moved home to Memphis to help take care of her and to help run her printing business. By Stephen Maing on Publish Date December 20, 2013.

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Regards,
     Greg_L-W
Greg Lance-Watkins

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If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
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Later in the sequence of my experiences with cancer you will note that I introduce some results and events most probably linked with cancer such as enlarged & damaged Prostate and a consequential Heart Attack leaving me with no right coronary artery!
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I have also included numerous articles and anecdotes regarding health – primarily related to cancer, prostate and heart conditions – FYI!
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Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
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YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help you in ANY way. .

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