NATURAL SYSTEM PUTS BRAKES ON OBESITY
Imagine a way to turn off fat so that "spare tires" and "thunder thighs" are a distant memory. Researchers at Rockefeller University in New York and the Joslin Diabetes Center in Boston report they are able to do that by manipulating a gene in obese mice. The gene, called Foxa-2, inhibits young body cells from becoming mature fat-producing cells called adipocytes. In addition, when this gene is switched on in mature adipocytes, it functions as a brake to slow down further fat production and storage. "We have shown that Foxa-2 has two beneficial effects in mice: it counter-regulates the formation of fat and it increases the activity of genes important for insulin sensitivity. This is the ideal combination for pharmacologically treating obese or type 2 diabetic patients, or people with a risk of developing obesity," says the lead investigator. The study will be published in the August 1 edition of the Journal of Clinical Investigation.
GENE LINKED TO DEPRESSION AND STRESS
The likelihood that stressful life events will trigger depression depends on the genetic hard-wiring of an individual. Researchers the University of Wisconsin and King's College London found individuals with the "short" version of the serotonin transporter gene have a higher risk of depression when experiencing multiple stressful events such as death of a loved one, loss of job or prolonged illness. This short gene also increases the likelihood of depression among adults who were abused as children. People with the "long" version of the gene experienced no more depression than people who experienced no stressful life events. The study followed 847 Caucasian New Zealanders from birth to adulthood. Among those experiencing 4 or more life stressors, 43 percent of those with two copies of the short variant developed depression compared to 17 percent of those with two copies of the long variant. The study was published in the July 18 issue of Science.
STUDY IDENTIFIES WHICH COLON CANCER PATIENTS BENEFIT FROM CHEMOTHERAPY
A simple genetic test can determine if chemotherapy will be effective in treating a patient's colon cancer. The study, conducted by researchers form Toronto's Princess Margaret Hospital and Mount Sinai Hospital, examined 570 tissue samples from colon cancer patients. They found patients with a specific mutation in their tumor, high frequency microsatellite instability, did not benefit from chemotherapy. "This study shows that the usual type of chemotherapy is effective for about 83 percent of colon cancer patients," said the study's lead author. Testing for this genetic mutation could become routine during diagnosis, with the results used to direct treatment of colon cancer. The study results were published in the July 16 issue of the New England Journal of Medicine.
GENETICS LINKED TO FALSE-POSITIVE TEST RESULTS IN PROSTATE CANCER
Genetics cause some men to test higher on the blood test for prostate cancer even when they don't have the disease. Researchers from Wake Forest University Baptist Medical Center, in conjunction with colleagues from St. Louis University and Washington University School of Medicine, analyzed blood samples from 405 Caucasian males, identifying three variations in part of the gene that controls prostate specific antigen (PSA) levels. The variations together contribute to a 30 percent increase in PSA levels, and research suggests that if a man has one variation, he has all three. "Up to 20 percent of men may have genetic variants that cause levels of PSA that are about 30 percent higher than other men, which could result in needless biopsies," said the lead researcher. According to the researchers, testing for the variants is quick and inexpensive, and could one day become part of the PSA screening process. The study was published in the July 16 issue of the Journal of the National Cancer Institute.
GENETIC ROAD MAP POINTS TO SOURCES OF DISEASE
Scientists produced a map that helps pinpoint genes linked to diseases such as diabetes, hypertension and schizophrenia. This linkage map, designed by researchers at Rutgers, is based on the amount of interaction taking place among nearly 3,000 genetic markers whose positions are known. The markers used for the map are called single-nucleotide polymorphisms, the variations of a gene that people carry at one point of their DNA. The lead researcher pointed out SNPs provide a shortcut for pinpointing genes that may contribute to disease because SNPs are both plentiful and easy to analyze. "It is anticipated that the successful identification of a set of SNPs tailored for linkage analysis, such as that presented here, will stimulate development of mass-produced (less expensive) means for large-scale genotyping with this same marker set," the researchers wrote in a paper describing the linkage map, which will be published in the August issue of the American Journal of Human Genetics.
(Editors: For more information on OBESITY GENE, contact Joseph Bonner at 212-327-8998 or bonnerj@Rockefeller.edu. For DEPRESSION, Jules Asher at 301-443-4536 or NIMHpress@nih.gov. For COLON CANCER, Vince Rice at 416-946-2000 or firstname.lastname@example.org. For PROSTATE, Karen Richardson at 336-716-4587 or email@example.com. For LINKAGE MAP, Joseph Blumberg at 732-932-7084 x652 or firstname.lastname@example.org)