报告人: Yun-Fai Chris Lau (刘润辉), Professor, Department of Medicine, School of Medicine, University of California, San Francisco, USA

报告时间：11月29日 上午9:30-11:30

报告地点：闵行校区生物药学楼1号楼105会议室

联系人: 吴际教授（jiwu@sjtu.edu.cn）

报告人简介：

Yun-fai Chris Lau received Ph.D. in Cell Biology (1979) from the University of Texas MD Anderson Cancer Center. Prof. Lau then worked as a Postdoctoral Fellow (1979-1982) at the University of California, San Francisco. Prof. Lau is an internationally recognized investigator in the field, particularly on sex determination and male-specific/dominant cancers and diseases. Prof. Lau was the Visiting Professor in several universities including Japan Academy, Tokyo, Japan. He was also the Organizer of International Meetings and Conferences and published over 120 research articles. Now, Prof. Lau is a member of Cancer Genetics Program, Prostate Cancer Program Helen Diller Family Comprehensive Cancer Center-UCSF. In addtion, Prof. Lau is the external reviewer or member of University Grant Council, Hong Kong and other professional sevice organizations, and the editor and member of journals including cell and Bioscience, Journal of Genetics and Genomics, Genes.

报告摘要:

The gonadoblastoma locus on the Y chromosome (GBY) harbors a gene, which predisposes the dysgenetic gonads of patients with disorders of sexual development (DSD) to develop gonadoblastoma. Our laboratory initially cloned the testis-specific protein Y (TSPY) gene, and subsequently demonstrated it to be the GBY gene. It has a homologous gene, TSPX on the X chromosome. TSPX and TSPY originated from the same ancestral gene, but diverged during the evolution of the human sex chromosomes, i.e. X and Y chromosome. Recently we demonstrated that TSPY and TSPX interact with the male sex hormone receptor, androgen receptor (AR) and its constitutively active variants, such as AR-V7, lacking the ligand-binding domain. Our results support the notion that the male-specific oncogene TSPY and the male sex hormone receptors form a positive feedback loop in the oncogenesis of various male-specific cancers and male-biased cancers and greatly amplify their synergistic actions in human cancers.