To test this hypothesis, w analyzed paired 60 lung adenocarcinomas and adjacent non-tumor tissues from patients who were less than 50, older than 79, or between 57-72 years of age at the time of diagnosis for the presence of LOH in five commonly affected chromosome arms including 3p, 3q, 9p, 17p, and 19p. This approach led use to identify a small region on ch. 3p as the region most strongly associated with patients who had lung cancers younger than age 50. In the past year, we identified a small set of candidate genes in this region as potetial targets of inactivation in lung tumors of early age onset patients. Our data is the first to provide direct evidence linking lung cancer susceptibility in extreme-age populations to a specific genetic alteration in the human genome. We are now sequence these candidate genes in primary tumors and the matched normal lungs to determine if genetic alterations in these genes might contribute to lung cancer development. Additional studies are also underway to determine the cellular location of these genes and their potential molecular function in cell growth and tumor formation.
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