Funded in partnership with the Lung Cancer Initiative of North Carolina, utilizing Stuart Scott Memorial Cancer Fund matching funds and the Richard Jones Fund for lung cancer
Lung cancer remains a major cause of cancer mortality worldwide, and in 2017, 155,870 people are expected to die from lung cancer in US. African Americans have the highest lung cancer incidence and lung cancer-related death rate and develop the disease at an earlier age compared to other racial groups. African Americans also have poorer survival, because of limited access to lung cancer screening, adequate healthcare, and appropriate therapeutic interventions. Etiology studies suggest that such a disparity in lung cancer may be due to genetic susceptibility, in addition to environmental exposures to cigarette smoking, radon, asbestos, and arsenic. Recently, we identified a novel gene, DCAF4, through a large-scale meta-analysis in Caucasian populations, which is likely to be involved in cell-cycle control and DNA damage response that is relevant to African Americans as well. Our hypotheses are that dysfunctional DCAF4 impacts cancer initiation and progression by altering multiple cellular processes and that DCAF4 functional variants alter gene expression and tumor cell phenotypes, which may explain racial disparity in lung cancer. Therefore, we proposed to study the functions of this gene and its risk-associated genetic variants on cellular phenotypes in lung cancer cells, animals and human clinical samples of lung cancer. We will test the hypotheses that dysfunctional DCAF4 impacts cancer initiation and progression by altering multiple cellular processes and that DCAF4 functional variants alter gene expression and tumor cell phenotypes. By including clinical samples from both Caucasians and African Americans, we hope to identify genetic markers for disparity in lung cancer.
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