Breast Cancer Risk Elevated in Male BRCA Mutation Carriers
Men with mutations in the BRCA1 or BRCA2 genes are at greater risk of breast cancer than the general population.
Male breast cancer accounts for less than 1 percent of all breast cancers in the U.S., and it is most common in men with a family history of the disease. Previous studies have shown that men who carry mutations in the BRCA2 gene have a greater risk of developing breast cancer than men in the general population. The association between BRCA1 mutations and breast cancer in men was less clear.
Sining Chen, Ph.D., of Johns Hopkins University and colleagues analyzed data from the National Cancer Institute’s Cancer Genetics Network on 1,939 families including 97 men with breast cancer.
The risk of developing breast cancer was higher in male BRCA1 and BRCA2 mutation carriers, compared with noncarriers, but BRCA2 mutation carriers had the highest risk. The relative risk was greatest for men in their 30s and 40s and decreased with age. The estimated breast cancer risk of a 70 year old male BRCA2 mutation carrier was 6.8 percent, compared with 1.2 percent for BRCA1 mutation carriers.
“Such risk estimates are important for determining appropriate risk management strategies for the male members of families with germline mutations in BRCA1 or BRCA2,” the authors write.
Contact: Tim Parsons or Kenna Lowe, public affairs office, Johns Hopkins School of Public Health, paffairs@jhsph.edu, (410) 955-6878
High Carb Diet Linked to Prostate Tumor Growth
A diet high in refined carbohydrates, like white rice or white bread, is associated with increased prostate tumor growth in mice.
Having too much insulin in the blood, a condition called hyperinsulinemia, is associated with poorer outcomes in patients with prostate cancer. Vasundara Venkateswaran, Ph.D., of Sunnybrook Health Sciences Centre in Toronto and colleagues investigated whether high insulin levels caused by eating a diet high in refined carbohydrates would lead to more rapid growth of prostate tumors in mice.
Forty mice were randomly assigned to either a high carbohydrate-high fat diet or a low carbohydrate-high fat one for nine weeks. The researchers measured the animals’ weight, tumor size, and insulin levels weekly. Mice on the high carbohydrate diet gained more weight, had faster growing tumors, and had higher insulin levels than mice on the low carbohydrate diet.
“Our results provide support for the concept that diets associated with a reduction in insulin level may have benefits for prostate cancer patients, particularly for the subset of patients who are hyperinsulinemic,” the authors write.
Contact: Vasundara Venkateswaran, vasundara.venkateswaran@sunnybrook.ca, (416) 480-6100 x 3127
Risk of HPV-Related Head and Neck Cancers Not Increased by Smoking and Drinking
HPV infection is associated with an increased risk of head and neck cancers, but that risk is not further heightened by tobacco or alcohol use.
This year an estimated 45,000 people in the U.S. will be diagnosed with head and neck cancers, which include cancers of the mouth and throat. Tobacco and alcohol use are thought to be the leading risk factors for head and neck cancers, but infection with human papillomavirus (HPV) is also associated with increased risk of these cancers.
Karl Kelsey, M.D., of Brown University in Providence, R.I., and colleagues examined the relationships between tobacco and alcohol use and HPV infection on the risk of head and neck cancers. They collected data on smoking habits, alcohol consumption, and HPV infection from 485 head and neck cancer patients and 549 control subjects residing in the Boston area.
Smoking was most strongly associated with cancer of the larynx (voice box), alcohol with mouth cancer, and HPV infection with throat cancer. Although smoking and drinking were associated with an increased risk of head and neck cancer, they did not further increase the risk of these cancers among people with HPV infections.
“Our results strongly support the emerging view that the etiology of [HPV-related head and neck cancers] is distinct from that of [head and neck cancer] tumors associated with smoking and drinking. This may have important implications for the treatment of [head and neck cancer],” the authors write.
Contact: Wendy Lawton, office of media relations, Brown University, wendy_lawton@brown.edu, (401) 837-6055
Drugs Improve Virus’ Cancer-Killing Power
Treatment with drugs that reduce the formation of new blood vessels may improve the efficacy of cancer-killing viruses.
Cancer-killing viruses look promising in laboratory tests, but they have had little success in treating human patients. Researchers suspect that the body’s immune responses and changes in the network of blood vessels surrounding the tumor may be inhibiting the viruses’ cancer-fighting abilities.
Balveen Kaur, Ph.D., of Ohio State University in Columbus and colleagues investigated how the viruses affect tumor blood vessels in rats with brain tumors. They also examined how changes to the tumor blood vessel network influence the viruses.
Treatment with the cancer-killing viruses was associated with a heightened immune response in the rats. This response was suppressed in rats that were given certain drugs that inhibit blood vessel growth, which allowed the viruses to work more effectively.
In an accompanying editorial, Jung Hyo Rhim, M.D., and Giovanna Tosato, M.D., of the National Cancer Institute in Bethesda, Md., describe how the use of viruses for treating cancer developed and how the tumor microenvironment, including the blood vessel network, has emerged as an important target for cancer treatments.
“As we learn more about the tumor microenvironment and its impact on tumor growth, we will be able to develop therapeutic strategies that combine specific tumor cell targeting as well as targeting the tumor microenvironment that facilitates tumor cell growth,” the editorialists write.
Contact:
*Article: Darrell Ward, associate director for cancer communications, Ohio State University Medical Center, darrell.ward@osumc.edu, (614) 293-4833 *Editorial: National Cancer Institute press office, ncipressofficers@mail.nih.gov, (301) 496-6641
Also in November 27 JNCI:
*http://www.eurekalert.org/emb_releases/2007-11/jotn-mp112007.php
*http://www.eurekalert.org/emb_releases/2007-11/jotn-im112007.php
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