But researchers at Weill Cornell Medical College have located a gene that could mutate to make Y. pestis resistant to many common drugs. Scientists believe that antibiotic-resistant Y. pestis should potentially concern the public and scientific community, because the bacteria might be used as a potential bioterrorism agent.

Dr. Luis Quadri, associate professor of microbiology and immunology at Weill Cornell Medical College, and his research team located the gene that, when overexpressed or in high numbers in the body, allows the bacterium to be almost bulletproof. The researchers scanned colonies of the bacterium E. coli, which had Y. pestis genome fragments implanted within, and found that some of the bacteria were able to resist the effects of multiple antibiotic drugs. Upon further inspection, the researchers found that these rare microbes contained high numbers of a Y. pestis gene called robA -- a gene that activates production of microscopic pumps that flush toxins and antibiotics from the cell. The greater the number of robA in Y. pestis, the more cellular pumps, and the easier it is for the bacterium to eliminate the antibiotics.

Because the findings' importance has generated above-average readership, the study has earned the permanent "Highly Accessed" distinction by the BioMed Central Microbiology site. To read a full-text copy of the study published in a recent issue of the journal BioMed Central Microbiology, please visit: www.biomedcentral.

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Because the Asian and white women reported similar numbers of affected relatives on average, it's possible that fewer Asians with the mutations go on to develop cancer. In that case, the family history would be a less accurate way to determine the presence of the mutations. Kurian and her colleagues are collaborating with researchers in Hong Kong to investigate these and other alternatives.

The study results point out the need for further investigation into the genetic variability of different ethnic groups. In addition to previously identified, clinically important mutations of the genes, the researchers identified more "variants of unknown significance" in the BRCA1 and BRCA2 genes of Asian women than in white women.

Many of these variants probably don't have any clinical effect," said Kurian. "We know a lot more about the normal variability of these genes in white women. Many of these variants are probably just normal for members of a particular ethnic group, but we haven't studied enough people in ethnic minority groups to know for sure, and further research needs to be done to distinguish variants of uncertain significance from truly harmful mutations."

Kurian's Stanford co-authors include Gail Gong, PhD, research associate; Nicolette Chun, MS, genetics counselor; Meredith Mills, manager of the Stanford Cancer Center's genetic counseling program; Ashley Staton, research assistant; Kerry Kingham, MS, genetics counselor; Dee West, PhD, professor of health research and policy at Stanford and chief scientific officer at the Northern California Cancer Center; Alice Whittemore, PhD, professor of health research and policy; and James Ford, MD, associate professor of oncology and of genetics. Other co-authors are from UCSF, Queen's Medical Center in Hawaii and British Columbia Cancer Agency in Ontario.

The study was funded by the Susan G. Komen Breast Cancer Research Foundation and the National Institutes of Health.

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