|Highlights from the annual meeting of the American Association for Cancer Research|
April 7, 2000
April 1-5, 2000, about 10,000 clinical and laboratory researchers interested in cancer met in San Francisco. Genetics is gaining an increasing role in the study of cancer, as highlights from meeting abstracts show.
How Helicobacter causes cancer
In the past decade, scientists were surprised to learn that ulcers arise not from stress alone, but from an infection with the bacterium Helicobacter pylori. Subsequent research has linked the bacterium to stomach cancer as well. But how does a bacterium cause cancer? Jae J. Kim and colleagues at the Baylor College of Medicine, Houston, report that the bacterium may directly affect a cellís DNA repair mechanism. They grew stomach cancer cells in the laboratory and challenged them with increasing doses of H. pylori. The levels of two DNA mismatch-repair proteins fell with increasing bacterial infection. The bacteria did not affect two control proteins. The researchers conclude that the H. pylori effect may represent a critical early event in the natural history of stomach cancer.
Prophylactic bilateral mastectomy protects against breast cancer
Women who test positive for mutations in the breast cancer genes BRCA1 and BRCA2 stand a 56 percent to 85 percent lifetime risk of breast cancer according to two large studies. A woman who tests positive has three options. She can choose watchful waiting, which means careful self-examination and frequent mammograms; she can take anticancer drugs such as tamoxifen; and, in some cases, she may decide to have both breasts removed prophylactically. Lynn C. Hartmann and colleagues at the Mayo Clinic in Rochester, Minnesota, studied 28 women with a family history of breast cancer, mutations in either BRCA1 or BRCA2 and who chose the latter course. The team has followed the women for an average of about 15 years. None of the women has been diagnosed with breast cancer. The team concludes that bilateral prophylactic mastectomy affords significant protection against breast cancer in women with mutations in either of the two genes.
Detecting prostate cancer from urine tests
Earlier detection of prostate cancer may come from studies of DNA in cells or parts of cells present in urine. Paul Cairns and colleagues at Fox Chase Cancer Center in Philadelphia, Pennsylvania and the Johns Hopkins Hospital in Baltimore, Maryland investigated a chemical compound that switches genes on and off. When methyl groups attach to the regulatory parts of genes, the genes remain silent; the cell does not translate them into protein. Cairns and colleagues focused on a gene called GSTP1, finding it was methylated in 79 percent of prostate tumors. They also showed for the first time that testing urine for methylated GSTP1 is a useful way to identify prostate cancer. Testing cell debris in urine samples from the patients with methylated GSTP1 in their prostate tumors, the researchers found that nearly a third of those urine samples also tested positive for methylated GSTP1. Although the urine test did not detect all prostate cancers, no false positive tests occurred. The researchers conclude that urine testing for prostate cancer is feasible and worth further development.
Estrogenís role in lung cancer
New research adds evidence to conflicting reports about the role of estrogen in the development of lung cancer. Jill Siegfried and colleagues at the University of Pittsburgh, Pennsylvania, reported that that the hormone plays a role in non-small-cell lung cancer. The researchers detected two estrogen receptor proteins in lung cancer cells grown in the laboratory. They conclude that estrogen may play a role in lung cancer similar to its role in breast cancer, and that production of the estrogen-receptor proteins may represent part of the progression of normal lung cells into tumor cells.
Genetic variation may help explain why alcohol causes throat cancerResearchers have theories but no sure explanation of how alcohol consumption contributes to cancers of the mouth and throat or how it interacts with tobacco. One possible explanation is acetaldehyde, a chemical produced during normal breakdown of alcohol. Two enzymes are involved in this chemical breakdown, and Simone Benhamou, of Inserm U521, Villejuif, France and an international group of colleagues examined variations, or polymorphisms, in the genes coding for these enzymes. Studying 250 cancer patients and 172 healthy people, all of whom smoked, the researchers found that polymorphisms in one of the two genes, called CYP2E1, may affect the risk of mouth and throat cancers. The heaviest drinkers who also had a particular polymorphism in the CYP2E1 gene had the highest risk of cancer.
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