DESCRIPTION (Applicant's Description) Lung cancer has been the leading cause
of death due to malignancy in the United States for decades. While
cigarette smoking has been identified as a major risk factor, it is known
that only a small proportion of all heavy smokers will develop lung cancer
eventually. Evidence of lung cancer familial aggregation suggests
variability in inherited susceptibility. Genetic polymorphisms in several
microsomal mixed-function oxidases and phase II detoxification enzymes, both
of which are important in the activation and detoxification of chemical
carcinogens, have been reported to affect risk of lung cancer. Genomic
alterations and instabilities have also been indicated for lung cancer risk
in the recent literature. In addition, studies of both smokers and
nonsmokers suggested overlapping etiology between lung cancer and selected
chronic pulmonary diseases. Thoroughly evaluating the intricate roles and
interactive effects of major susceptibility gene(s), risk modifier gene(s),
and exogenous carcinogens requires a comprehensive study design and data
resource which integrates the traditional epidemiologic approaches and newly
developed genetic and molecular tools. The purpose of this protocol is to
identify newly diagnosed lung cancer patients seen at Mayo Clinic and to
build a patient, family and biosample resource for a comprehensive
genetic-epidemiologic study of lung cancer. From the estimated 3,840 lung
cancer patients newly diagnosed at the clinic between 1/1/1995 and
12/31/1998, 1,118 will be identified as study subjects. There are 250
Olmsted county residents anticipated for population-based studies. Data on
approximately 900 selected clinical-based patients will be available for the
following genetic and molecular epidemiologic studies: (1) 384 patients
with positive family history of lung cancer and 152 patients with strong
family history of cancer in general will be ascertained for identifying lung
cancer susceptibility gene(s); (2) 190 nonsmoking and 114 young-age (50
years old at diagnosis) patients will be identified for investigating the
causes other than or in addition to tobacco smoking; (3) 100 sporadic cases
who are smokers older than 50 years will also be included as an internal
comparison group. Thus, the developed data resource will enable us to
further test and locate the lung cancer susceptibility gene and its
interaction with other genes and tobacco exposure. A specific hypothesis,
i.e. whether lung cancer is associated with alpha-1 antitrypsin deficiency
heterozygous status, will be tested in this proposed study.
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