Lung cancer is the epitome of an environmentally induced disease.
Eighty-seven percent of lung cancers are attributed to tobacco
exposure. However, only a fraction of smokers develop neoplastic
lesions. Genetically determined modulation of environmental exposures is
an attractive possible mechanism for the variation in host susceptibility.
In vitro chromosomal analyses have been frequently used to study
individual sensitivity to genotoxicity and cancer risk. Screening of
peripheral blood lymphocytes (PBLs) for cytogenetic defects has proven
useful in studying other cancers. Deletion of chromosome 9p has been
reported in numerous tumor types, especially lung cancer. We have
shown that spontaneous chromosome aberrations on chromosome 9 in
PBLs were a significant risk predictor for lung cancer. This proposal is
designed to build upon those preliminary data and within the recently
funded lung-cancer SPORE study which involves collaboration among
investigators in basic, clinical, and public-health sciences at The
University of Texas Southwestern medical Center and M.D. Anderson
Cancer Center. The ongoing study is integrating epidemiologic data with
molecular susceptibility factors in patients with newly diagnosed lung
cancer to determine the extent of host factors that predispose to lung
cancer risk. The specific aims of this proposed supplementary study
1. To determine the relationship between family history of lung cancer
and spontaneous chromosome aberrations in PBLs of 00 lung cancer
patients with (cases) and 100 without a family history of lung cancer
(controls). Our working hypothesis is that spontaneous chromosome
aberrations reflect genetic instability and that individuals with such
aberrations are more likely to report a family history of cancer than
individuals without such aberrations. Chromosome 9 aberrations may be
a marker of cancer susceptibility and may be associated with familial
aggregation of cancer.
2. To access the associations between the genetic marker and age,
cigarette smoking status, and nutrition status by integrating
epidemiologic data with the cytogenetic, molecular cytogenetic, and
molecular genetic data. Our hypothesis is that spontaneous chromosome 9
aberrations in PBLs are inherited genetic defects that are not associated
with specific exposures. These data are being routinely collected in
SPORE Project 2.
The long-term goal of this study is to further our understanding of
lung carcinogenesis. Chromosome 9 aberrations may be useful as
biomarkers to identify high-risk populations. Because it builds on an
existing study of lung cancer, this proposal is both time and cost
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