60周年校庆暨院庆系列学术报告：2018.06.07 Zhiyuan Shen 教授（Rutgers Robert Wood Johnson Medical School ）学术报告会
题目: Genomic Instability and Tumorigenesis: Confounding roles of essential caretaker genes 报告人：Dr. Zhiyuan Shen Rutgers Robert Wood Johnson Medical School 邀请人：姚雪彪 教授 时间： 2018.6.7（周四），下午16:00 地点：生命科学学院329B会议室 报告人简介： Dr. Zhiyuan Shen is a professor in the Department of Radiation Oncology and Department of Pharmacology at the Rutgers Robert Wood Johnson Medical School, and an adjunct professor at the Department of Genetics of the Rutgers School of Arts and Sciences. Dr. Shen received a MD degree from the Norman Bethune University of Medical Sciences (now merged with Jilin University, China) in 1985, and a PhD degree in Molecular Biology and Radiation Biology from Colorado State University in 1993. After completing a Director’s Postdoctoral Fellowship at the Los Alamos National Laboratory, he became an tenure track Assistant Professor at the University of Illinois at Chicago (1997), and at University of New Mexico (2000) where he was promoted to Associate Professor with tenure in 2003. In 2006, he was recruited to Rutgers Cancer Institute of New Jersey (CINJ) as the inaugural chief of the newly formed Division of Radiation Cancer Biology within the Department of Radiation Oncology. In 2008, he became a tenured full professor and was appointed a co-leader of the previous Genomic Instability and Tumor Progression and the current Genomic Instability and Cancer Genetics research program at Rutgers Cancer Institute. Dr. Zhiyuan Shen has a longstanding interest to elucidate the mechanisms by which genomic instability is provoked and how it drives tumorigenesis. Works from his laboratory suggests that BCCIP plays a critical role in multiple mechanisms that maintain genomic integrity and regulate cell proliferation. Recently, Dr. Shen has devoted a significant effort to establish unique mouse models and genomic approaches to reveal new mechanism by which caretaker genes maintain genomic integrity and suppress tumorigenesis.
报告摘要： Genes that maintain the stability of the genomes are often considered caretaker tumor suppressors. Defects of this class of tumor suppressors often lead to mutator phenotypes and drive genomic instability and tumorigenesis. However, many of the caretakers are also essential for DNA replication, mitosis, and cell viability. Thus defects of caretakers can lead to impaired cell proliferation and may prohibit tumorigenesis. In this presentation, I will use BCCIP, a BRCA2 and CDKN1A/p21 Interacting Protein, as an example to discuss how dis-regulations of essential caretakers contribute to tumorigenesis, and to update on our understanding of BCCIP functions in DNA repair, replication, and mitosis.