A team from the chemistry and biology departments of New York University, in collaboration with Memorial Sloan Kettering Cancer Center (MSKCC), has uncovered a conformational switch--a change in shape in a carcinogen-damaged DNA site--in tumor suppressor genes altered by a known cancer-causing chemical found in cigarette smoke. This finding may open new horizons for understanding the initiation of chemically induced cancers.
The findings appear as the cover story in the latest issue of the Journal of Molecular Biology. This team was headed by Dinshaw Patel at MSKCC, Nicholas Geacintov, chair of NYUs chemistry department, and Suse Broyde, a professor in NYUs biology department.
The studied gene, p53, is an important tumor suppressor gene that plays critical roles in cellular functions such as cell-cycle control, differentiation, and DNA repair. Many different chemical carcinogens, including those that are primary components of cigarette smoke, are known to damage DNA. This damage occurs at special positions of the p53 gene, called mutation hot spots, which have been previously linked with cigarette smoke. This molecular link between chemical DNA damage and cigarette-associated lung cancer has been called the "smoking gun."
James Devitt | EurekAlert!
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