报告题目：Liver cancer research, from mechanism to combination immunotherapy 报 告 人：Gen-sheng Feng Ph.D.,Professor,Section of Molecular Biology,Division of Biological Sciences,University of California,San Diego 主 持 人：张灼华 教授 报告时间：2019年7月30日（星期二）上午10:30 报告地点：中南大学医学遗传学研究中心老楼五楼报告厅 Gen-sheng Feng(https://biology.ucsd.edu/research/faculty/gfeng#research-tab) Biography Dr. Feng received his PhD degree at Indiana University Bloomington and did a postdoctoral fellowship at the University of Toronto. Research Molecular Signaling in Cancer, Metabolism and Stem Cells At the heart of cancer research is the elucidation of oncogenes and tumor suppressor genes (or anti-oncogenes), which has been a driving force in the cancer field for several decades. Most recent studies in this and other labs have revealed dual roles of genes in promoting and suppressing hepatocellular carcinoma (HCC). Deciphering the “paradoxical” effects of these genes may provide a fresh view on the fundamental mechanisms of carcinogenesis, which can lead to development of mechanism-based therapeutics for HCC. Our current focuses are on delineating genetic and epigenetic interactions and cell-cell communications that drive hepatocarcinogenesis. We are very interested in isolating and characterizing cancer stem cells, CSCs (or tumor-initiating cells, TICs) in the liver, and in dissecting the dynamic interplay between tumors and the hepatic microenvironment. Efforts are also being devoted to elucidation of metabolic changes in tumor cells and to search of biomarkers for early diagnosis of liver cancers. We are also interested in deciphering the common and distinct biochemical pathways in self-renewal of hematopoietic stem cells (HSCs) and leukemia stem cells (LSCs), with the objective of understanding how an HSC pool is maintained throughout life, and with the ultimate goal of identifying novel targets for elimination of LSCs. Another focus is on dissecting the signaling events involved in metabolic disorders such as obesity and diabetes. Ongoing experiments are aimed at understanding the intertwining of leptin and estrogen signaling cascades, to illustrate why estrogen has a leptin-like effect in control of metabolism, why postmenopausal women have the tendency to develop obesity, and why obesity promotes breast cancer. Whereas obesity has become a serious health problem in developed countries worldwide, one ongoing project in the lab is to investigate an indispensable physiological role of adipogenesis and adipose tissue in mammals, as revealed by the most recent data obtained in this lab.