报告地点：闵行生科院534报告厅

报告人简介：Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee

报告摘要：The intrinsic resistance to DNA-damaging therapies is a hallmark of esophageal adenocarcinoma (EAC). Cisplatin (CDDP, cis-diamminedichloroplatinum) exerts its cytotoxic effect by inducing DNA damage and causing apoptosis through activation of p53 or p73 proteins. A previous study showed that cisplatin increased p73 protein levels through activation of the non-receptor tyrosine kinase c-ABL. Cisplatin is currently used as a first-line therapy in patients with EAC, but resistance remains a serious clinical challenge. The AXL receptor tyrosine kinase has been associated with cell survival, proliferation, and migration in solid tumors. The aim of this study was to investigate the role of AXL in mediating CDDP resistance in EAC and identify the underlying molecular mechanism.