NYU and MSKCC research provides model for understanding chemically induced cancer ...( nformational differences in methylated ...)

NYU and MSKCC research provides model for understanding chemically induced cancer initiation

nformational differences in methylated and unmethylated DNA sequences may be significant because of potential alterations in the cellular processing of these lesions by DNA transcription, replication, and repair enzymes," said NYU's Geacintov.

"Because environmental chemical carcinogens, including those present in cigarette smoke, are a significant threat to human health, it is imperative to understand how chemicals can induce mutations and cancer at the molecular level," added NYU's Broyde. "Such information is needed for devising novel preventive and therapeutic strategies for addressing the problem of cancer induction by environmental chemical carcinogens."

The researchers added that the finding opens new horizons, at the molecular level, for understanding the effects of methylation at p53 mutation hot spots on the properties of carcinogen-DNA lesions. Current thinking in the field of chemical carcinogenesis is that the mutation-prone, or error-free processing of such carcinogen-damaged p53 genes by DNA repair proteins and DNA and RNA polymerases can determine whether these lesions ultimately contribute to the development of lung and other cancers.

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Contact: James Devitt
james.devitt@nyu.edu
212-998-6808
New York University
9-Mar-2005

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