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Principal Investigator
Chengguo Xing
University of Florida
Position Title
About this CDAS Project
PLCO (Learn more about this study)
Project ID
Initial CDAS Request Approval
Oct 8, 2020
Biological bases of lung cancer risk disparities for African American male smokers
Disparity exists in lung cancer risk that African American (AA) male smokers have the highest risk. Given the limited success in lung cancer management, it is important to understand the molecular bases of lung cancer risk disparities, which will identify opportunities to improve its management. Tobacco use is the key risk factor for lung cancer. NNK is one of the best characterized tobacco specific pulmonary carcinogen with plenty of human data to support its role in human lung cancer incidence. At the same time, neurological conditions, such as stress, anxiety and depression, have been observed in epidemiological studies to increase cancer risk, particularly lung cancer. We hypothesize that the differences in tobacco exposure, tobacco carcinogen NNK uptake, tobacco carcinogen NNK activation, and psychosocial stress collectively contribute to the increased lung cancer risk among AA smokers, which are supported by our limited preliminary data of eight sets of biomarkers in the urine and plasma samples from AA and Caucasian American (CA) smokers. These biomarkers were selected for investigation because they respectively reflect tobacco exposure, tobacco carcinogen uptake, tobacco carcinogen activation and the level of mental stress. In order to rigorously test our hypothesis and to help reduce such a disparity in the future, we will quantify these biomarker candidates in additional plasma and urine samples from AA and CA male smokers, define their differences between AA and CA smokers, explore their correlations, and develop an integrated risk factor based on these multiple complementary biomarkers using a common factor model that may differentiate lung cancer risk disparities between AA and CA male smokers. We will also optimize our current analytical methods to improve their sensitivity, reproducibility and more importantly compatibility for future analysis of samples collected from the prospective clinical trials such as the PLCO plasma samples. The results are expected to expand our basic knowledge of tobacco exposure-induced lung carcinogenesis and elucidate the mechanisms responsible the disparities in lung cancer risk etiology. We also expect that the mechanistic insights will identify new opportunities for lung cancer prevention by identifying the high risk individuals.

1. To determine the rate of lung cancer incidence in AA smokers
2. To determine the rate of lung cancer incidence in CA smokers