"Cancer in the News"

CANCER_DISPARITIES_NEWS_DIGEST.doc

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Health in the communty
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Yahoo! News

Mutations in the BRCA1 and BRCA2 genes that increase the risk of breast cancer for women also do the same in men.

Men can develop breast cancer, although they account for only about 1 percent of breast cancer cases. Previous studies have shown that men who carry mutations in the BRCA2 gene are at greater risk of developing breast cancer than men in the general population. Now, new research suggests that the same is true for men with BRCA1 mutations.

Dr. Sining Chen from Johns Hopkins School of Medicine in Baltimore, Maryland, and colleagues studied data on 1,939 families that included 97 male patients with breast cancer.

“At all ages, the cumulative risks of male breast cancer were higher in both BRCA1 and BRCA2 mutation carriers than in noncarriers,” the researchers report in the Journal of the National Cancer Institute.

The likelihood of developing breast cancer was highest for men in their 30s and 40s and decreased with increasing age. For example, for BRCA2 mutation carriers, 30-year-old men were 22 times more likely to develop breast cancer than carriers at 70 years of age.

The risk was higher for BRCA2 than BRCA1 mutation carriers. The investigators calculate that, by age 70, the chances of developing breast cancer are 1.2 percent for male BRCA1 mutation carriers and 6.8 percent for men with the BRCA2 mutation.

They point out that these estimates of risk are “important for determining appropriate risk management strategies” for male members of families with mutations in BRCA1 or BRCA2.

SOURCE: Journal of the National Cancer Institute, December 5, 2007.

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Why Don’t All Moles Progress To Melanoma?
ScienceDaily (Oct. 5, 2006) — Everyone has moles. Most of the time, they are nothing but a cosmetic nuisance. But sometimes pigment-producing cells in moles called melanocytes start dividing abnormally to form a deadly form of skin cancer called melanoma. About one in 65 Americans born this year will be diagnosed with melanoma at some point during their lifetime.

Scientists know that 30 percent of all melanomas begin in a mole. They know that 90 percent of moles contain cancer-causing mutations. What scientists didn’t know is how melanocytes stop these mutations from triggering the development of cancer.
Maria S. Soengas, Ph.D., and other scientists in the Multidisciplinary Melanoma Clinic at the University of Michigan Comprehensive Cancer Center, have found the answer to this important question in an unexpected place—a structure inside cells called the endoplasmic reticulum, or ER.
“Our results support the direct role of the endoplasmic reticulum as an important gatekeeper of tumor control,” says Soengas, who is an assistant professor of dermatology in the U-M Medical School. “Until now, no one knew there was a connection between ER stress and the very early stages of tumor initiation.”
Results of the U-M study—involving melanocytes from normal human skin and biopsies of non-malignant human moles—are being published in the October issue of Nature Cell Biology.
The endoplasmic reticulum is the cell’s protein production factory. The process begins when chains of amino acids are deposited in the ER membrane in response to coded instructions from genes. Chaperone proteins fold these amino acids into specific shapes. When too many of them build up in the membrane, or when something goes wrong with the folding process, the system gets bogged down. This can stress or even kill the cell.
To prevent this, the ER sends out distress signals to activate what scientists call the unfolded protein response (UPR). This slows the protein production process and gets rid of excess incoming amino acids, giving the ER a chance to catch up. If that doesn’t work, the UPR causes the cell to destroy itself in a process called apoptosis.
“Traditionally, the ER’s role was considered to be limited to protein folding or protein modification,” Soengas says. “But scientists like Randal Kaufman, a U-M professor of biological chemistry and co-author on our paper, have found that the ER can sense changes in glucose, nutrients, oxygen levels and other aspects of cellular physiology associated with diseases like diabetes and Alzheimer’s disease.”
“In our study, we found that the ER senses the activity of certain oncogenes in the melanocyte and triggers a response that prevents the malignant transformation of these cells,” Soengas adds.
According to Soengas, the tumor suppressive mechanism induced by the ER in melanocytes with these cancer-causing mutations is premature senescence—a form of “suspended animation” that stops the cell cycle and keeps cells from dividing, but doesn’t kill them.
“The cells are held in check—they don’t die, but they don’t proliferate either,” Soengas explains. “In the case of moles, melanocytes can stay this way for 20 to 40 years or even your whole life. For most of us, just holding cells in an arrested state is sufficient to prevent the development of cancer. That’s why so many people have moles, but few have melanoma.”
In the study, U-M scientists found that the tumor suppressive response in melanocytes varied depending on the type of oncogene being expressed in the cell.
“We found that some oncogenes activated the endoplasmic reticulum, while other oncogenes didn’t,” Soengas says.
In a previous study, Soengas and colleagues found that certain oncogenes use a different senescence mechanism, which doesn’t activate the ER, to block the transformation of melanocytes. Both these mechanisms work in addition to or independent from other well-known tumor suppressor mechanisms involving apoptosis.
Soengas says the results of the study will be important in helping scientists understand all the different mechanisms melanocytes use to protect themselves against oncogenes. But she cautions that there are no immediate clinical applications for the study and additional research will be required.
In future research, Soengas will attempt to determine exactly how oncogenes trigger the unfolded protein response in malignant and non-malignant skin cells. “By comparing what happens in normal melanoctyes with what happens in melanoma, we may be able to come up with events that are specific for tumor cells, which could be used for future drug development,” she says.
Adapted from materials provided by University of Michigan Health System.