DESCRIPTION (Adapted from the Investigator's Abstract): To reach the
National Cancer Institute's goal of reducing cancer mortality 50% by the
year 2000, significant progress will have to be made in the prevention of
lung cancer, the leading cause of U.S. cancer mortality among both men and
women. However, even among individuals with chronic environmental
exposures, such as long term cigarette smoking, the risk of lung cancer is
relatively low. Preliminary studies suggest that this risk is unevenly
distributed, with certain individuals and families having much greater risks
of lung cancer development. Such clustering in families suggests that
genetic susceptibility may be a factor in carcinogenesis.
Previous studies have identified a number of genes that may influence
susceptibility to lung cancer. These loci are felt to mediate lung cancer
risk through the detoxification of (or failure to detoxify) common
environmental agents such as cigarette smoke. The primary goal of this
study is to relate lung cancer susceptibility in individuals and families to
DNA based variation among selected candidate detoxification loci. The study
will identify new DNA-based variation in an extended collection of
detoxification genes which may mediate the carcinogenic effects of exogenous
and endogenous lung cancer-related exposures. This variation will be
developed into assays that permit high-throughput characterization. Once
identified, tests for association of variation in candidate loci in cases
when compared to sex-matched controls who are smokers and non-smokers, will
be conducted. Assessment of association dependent on case characteristics
will be made. Using the family history information obtained from each case
and control reference individual, the patterns of cancer aggregation in
families will be assessed. Finally, the relationship between aggregation
with families and variation of candidate genes in probands and their family
members will be determined.
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