Time：10:00-11:30 AM, Wednesday, September 25，2024

    Host：Dr. Duanqing Pei, Chair Professor, School of Life Sciences

    Venue：Room E10-216, Yungu Campus

Speaker:

Dr. Vinay Tergaonkar, Distinguished Principal Scientist, Institute of Molecular and Cell Biology (IMCB), Singapore

Vinay Tergaonkar obtained his Ph.D. (2001) through an international cancer society (UICC) fellowship for collaborative research at Tufts University, Boston, USA. He has been a fellow (2001-2004) and a special fellow (2004-2006) of the Leukemia and Lymphoma Society of America and conducted his postdoctoral studies at the Salk Institute for Biological Studies, La Jolla, California. He joined Institute of Molecular and Cell Biology (IMCB), Singapore, in late 2005 as Principal Investigator and became a Senior Principal Investigator in 2010, Research Director in 2015. Since 2022, he is a Distinguished fellow of A*star. He is also a Professor at School of Medicine at National University of Singapore. Work from his laboratory has led to his inclusion (by Stanford University) in the top 2 % of the most cited scientists globally, and international recognitions including the British council development award (2014), the Premiers’ fellowship from Government of South Australia (2015)and distinguished visiting Professorships at Ashoka University and University of Macau. He serves on Editorial Boards of 1) Science Advances (AAAS), 2) Molecular and Cellular Biology (American Society for Molecular Biology), 3) Biochemical Journal (Portland Press). 

Abstract:

Over 90% of human cancers attain immortality by transcriptional re-activation of an enzyme called telomerase reverse transcriptase (TERT). While human germ and stem cells transcribe TERT, its expression is transcriptionally silenced in all somatic cells. How and why TERT is reactivated in the vast majority of human cancers remain fundamental unsolved problems in biology. I will present unpublished results which will suggest why TERT is reactivated in human cancers. I will also describe a molecular mechanism which explains how genetic and non-genetic factors, like high iron-(Fe3+), from consumption of red meat, collude to re-activate this enzyme, thereby explaining a long standing link between red meat and carcinogenesis. I will also describe the identification of a small molecule inhibitor of this molecular pathway that may be developed using medicinal chemistry for therapeutic use in a large proportion of human cancers where iron-(Fe3+) is a key driver. 

Contact：

Wenyue Yu: yuwenyue@westlake.edu.cn

School of Life Sciences