Molecular Epidemiology and Molecular Carcinogenesis of H

基因-环境相互作用是人类癌症分子流行病学中的一个重要概念。我们的病例对照（使用基于医院和人群的对照）研究集中于肺癌（一种与烟草相关的癌症）和结肠癌（一种与慢性炎症相关的癌症类型）。这些研究需要整合对癌症易感性遗传变异的日益加深的理解、对致癌物暴露的分析、快速发展的技术、生物信息学、社会伦理问题和流行病学研究设计方法。我们发现，对DNA损伤有反应的G2/M细胞周期检查点缺陷（一种表型特征）与非裔美国人比白种人患肺癌的风险更高有关。某些炎症细胞因子基因的基因型多态性，如IL-1a和IL-10，也与肺癌有关。我们正在继续我们长期以来对人类肺癌发生的研究。腺癌的分子特征确定了吸烟与非吸烟相关的癌症以及短期与长期幸存者。我们还发现了microrna的分子图谱，非蛋白质编码基因识别肺癌，其不同的组织学类型和预后。

Gene-environment interaction is a seminal concept in molecular epidemiology of human cancer. Our case-control (using hospital- and population-based controls) studies focus on lung cancer, a tobacco-related cancer, and colon cancer, one of the cancer types associated with chronic inflammation. These studies require the integration of an increasing understanding of genetic variation in cancer susceptibility, analysis of carcinogen exposure, rapidly developing technologies, bioinformatics, social-ethical concerns, and epidemiological study-design methods. We have discovered that a deficient G2/M cell cycle checkpoint that responded to DNA damage, a phenotypic trait, is associated with a higher lung cancer risk in African-Americans than in Caucasians. Genotypic polymorphisms of certain inflammatory cytokine genes, e.g., IL-1a and IL-10, were also associated with lung cancer. We are continuing our longstanding studies of human lung carcinogenesis. The molecular profile of adenocarcinoma identified smoking- versus nonsmoking-associated cancers and short-term versus long-term survivors. We have also discovered molecular profiles of microRNAs, nonprotein coding genes that identify lung cancer, its different histological types and prognosis.