Breast cancer gene not linked to higher risk of death

Young women with the BRCA gene mutation that prompted an actress pre-emptive and much-publicised double mastectomy are not more likely to die after a breast cancer diagnosis, scientists said.

In fact, they may have a "survival advantage" over non-carriers if diagnosed with triple-negative breast cancer, a form that is particularly hard to treat, a team wrote in the journal.

"Women diagnosed with early breast cancer who carry a BRCA mutation are often offered double mastectomies soon after their diagnosis or chemotherapy treatment" compared to non-mutation carriers, study co-author said in a statement.

"Our findings suggest that this surgery does not have to be immediately undertaken along with the other treatment."

According to the doctors, women with a mutation in the BRCA1 or BRCA2 genes have a seven-in-10 chance of getting breast cancer by the age of 80. They are also more likely to get it at a younger age than other women.

In 2013, a Hollywood star announced she had had both breasts surgically removed as a preventative measure after tests revealed she carried the mutation, despite not having been diagnosed with cancer.

For the new study, the team recruited 2,733 women aged 18-40 who had been diagnosed with breast cancer between 2000 and 2008.

Twelve percent of the women had a BRCA mutation.

The team tracked the women's medical records for an average period of just over eight years, and found that 651 of 678 total deaths were due to breast cancer.

"The study found that there was no difference in overall survival two, five or ten years after diagnosis for women with and without a BRCA mutation," a press statement said.

In a subgroup of women with triple-negative breast cancer, those with a BRCA mutation had slightly higher survival rates for the first two years after diagnosis.

"In light of their findings the authors suggest that women with triple-negative breast cancer and a BRCA mutation who choose to delay additional surgery for 1-2 years to recover from their initial treatment should be reassured that this is unlikely to affect their long-term survival," the statement said.

"However, risk-reducing surgery will still likely be beneficial for BRCA mutation carriers to prevent another new breast or ovarian cancer from developing in the longer term." While only about five percent of breast cancers are diagnosed in women younger than 40, a high proportion of deaths fall in this age category.

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Ovarian cancer could originate in the fallopian tubes, not the ovaries

Most — and possibly all- ovarian cancers do not start in ovaries but instead in the Fallopian tubes,   which are attached to them, claims a recent study. The new findings also point to the possibility that removing a woman’s Fallopian tubes, but not her ovaries, may reduce risk of ovarian cancer in those at high risk for disease, including those with genetic changes (mutations) known to increase risk (e.g. BRCA).

Senior study author said that based on a better understanding of its origins, the study suggests new strategies for the prevention and early detection of ovarian cancer. The results revolve around the Fallopian tubes, which enable egg cells that have the potential to be fertilised and become embryos to pass from the ovaries where they are made to the uterus.

The new study found that ovarian cancer cells have more in common with cells covering the tips of Fallopian tubes than with those on the surface of ovaries. If bio-markers can be found for these tubal cells, then according to researchers, future blood tests, advanced Pap smears, or direct tests on tubal tissue might be able to detect the ovarian cancer earlier.

“We are one of several centres taking part in Women Choosing Surgical Prevention or WISP trial, which seeks to determine whether removing the tubes improves quality of life, compared to removing both the tubes and ovaries,” Dr. stated. Despite the remaining uncertainties, the current study does confirm previous results that had suggested that many high-grade serious cancers in the pelvis are preceded by abnormal cells (lesions) occurring in the Fallopian tubes, called serous tubal intra-epithelial carcinoma (STIC).

Cancer cells may arise from nearby tissue or may have spread to a location from another part of the body, but their genetic profile reflects the tissue of origin. Thus, the researchers knew going in that if STIC cells and ovarian cancer cells had different genetic profiles, they must have originated in different tissue types. Instead, in-depth molecular analyses of cells from 96 women with high-grade serous carcinoma failed to identify any genetic differences between cancer cells arising in the tubes and serous “ovarian” cancers occurring elsewhere in the pelvis.

They found no differences in the 20,000 genes that they can identify. “This leads us to believe that these ovarian cancers all originate in the Fallopian tubes,” Levine noted. Ovarian cancer is more aggressive than many other cancers because it is hard to diagnose in its earliest and most treatable stages.

Fewer than 50% of women diagnosed with the disease survive for longer than five years after their diagnoses, according to a study.

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Changes in gene contribute independently to breast and ovarian cancer

Defects in a key gene - long thought to drive cancer by turning off the protection afforded by the well-known BRCA genes - spur cancer growth on their own, according to a study led by researchers from NYU Langone Medical Center.

The study gene, known as EMSY, has some of the same functions as BRCA1 and BRCA2, which are known to protect against breast and ovarian cancer when normal. When defective, BRCA genes block the body's self-defense against cancer-causing genetic mistakes.

The new study, published online Jan. 13 in Oncotarget, helps to explain why some women with healthy BRCA1 and BRCA2 genes develop cancer. The findings may also expand treatment options for the roughly 11 percent of women with breast and ovarian cancer and normal BRCA genes, say the study authors.

"Now that we know exactly how changes in EMSY spur cancer cell growth, we can start to design therapies to specifically target that activity and hopefully stop it," says senior author Douglas Levine, MD, director of the Division of Gynecologic Oncology at NYU Langone and its Perlmutter Cancer Center.

"This work also suggests that treatments that work for patients with BRCA1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar," says first study author Petar Jelinic, PhD, a research assistant professor at NYU Langone. "The best way to go rapidly from bench to bedside is to find new ways to use existing treatments."

When normal, EMSY, BRCA1 and BRCA2 give the body's cells instructions to create proteins that help to repair DNA damage that can cause cancer. When those genes are altered, the repair process fails and cancer grows. Overly active EMSY, like mutated BRCA1 or BRCA2, changes those instructions, so that the DNA damage repair process is blocked.

This new study dispels prior theories that EMSY's activation merely turned off the cancer suppression function of BRCA2, says Jelinic.

Earlier work by Levine and others pointed toward EMSY activation as a culprit in breast and ovarian cancer, but had only examined certain parts of the EMSY protein. The new study was the first to evaluate the full-length EMSY protein and to show that it acts independently of BRCA1 or BRCA2.

Furthermore, the research revealed the part of the EMSY protein is changed by an enzyme called protein kinase A. When there is more active EMSY than normal, this enzyme reacts with the EMSY protein to more thoroughly suppress the DNA repair process.

Breast cancer is the second most common cancer among women in the United States, after skin cancer. Ovarian cancer is the fifth leading cause of cancer death among women, according to the National Cancer Institute.




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Defects in a key gene - long thought to drive cancer by turning off the protection afforded by the well-known BRCA genes - spur cancer growth on their own, according to a study led by researchers from NYU Langone Medical Center.

The study gene, known as EMSY, has some of the same functions as BRCA1 and BRCA2, which are known to protect against breast and ovarian cancer when normal. When defective, BRCA genes block the body's self-defense against cancer-causing genetic mistakes.
The new study, published online Jan. 13 in Oncotarget, helps to explain why some women with healthy BRCA1 and BRCA2 genes develop cancer. The findings may also expand treatment options for the roughly 11 percent of women with breast and ovarian cancer and normal BRCA genes, say the study authors.
"Now that we know exactly how changes in EMSY spur cancer cell growth, we can start to design therapies to specifically target that activity and hopefully stop it," says senior author Douglas Levine, MD, director of the Division of Gynecologic Oncology at NYU Langone and its Perlmutter Cancer Center.
"This work also suggests that treatments that work for patients with BRCA1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar," says first study author Petar Jelinic, PhD, a research assistant professor at NYU Langone. "The best way to go rapidly from bench to bedside is to find new ways to use existing treatments."
When normal, EMSY, BRCA1 and BRCA2 give the body's cells instructions to create proteins that help to repair DNA damage that can cause cancer. When those genes are altered, the repair process fails and cancer grows. Overly active EMSY, like mutated BRCA1 or BRCA2, changes those instructions, so that the DNA damage repair process is blocked.
This new study dispels prior theories that EMSY's activation merely turned off the cancer suppression function of BRCA2, says Jelinic.
Earlier work by Levine and others pointed toward EMSY activation as a culprit in breast and ovarian cancer, but had only examined certain parts of the EMSY protein. The new study was the first to evaluate the full-length EMSY protein and to show that it acts independently of BRCA1 or BRCA2.
Furthermore, the research revealed the part of the EMSY protein is changed by an enzyme called protein kinase A. When there is more active EMSY than normal, this enzyme reacts with the EMSY protein to more thoroughly suppress the DNA repair process.
Breast cancer is the second most common cancer among women in the United States, after skin cancer. Ovarian cancer is the fifth leading cause of cancer death among women, according to the National Cancer Institute.


Read more at: https://medicalxpress.com/news/2017-01-gene-contribute-independently-breast-ovarian.html#jCp