Test for Sam W. Lee, Ph.D

Principal Investigator, Biologist - Massachusetts General Hospital Cutaneous Biology Research Center Professor MGH/Harvard Medical School Principal Investigator, Biologist - Massachusetts General Hospital Cutaneous Biology Research Center Professor MGH/Harvard Medical School Principal Investigator, Biologist - Massachusetts General Hospital Cutaneous Biology Research Center Professor MGH/Harvard Medical School Principal Investigator, Biologist - Massachusetts General Hospital Cutaneous Biology Principal
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617-522-3113

Overview

Massachusetts General Hospital
Cutaneous Biology Research Center
Building 149, 13th Street
Charlestown, MA 02129
617 726-6691

E-mail:
sam.lee@cbrc2.mgh.harvard.edu

Research description

Since my years as a Harvard faculty member, I have focused a sustained effort toward cancer biology, and my initial most significant contribution was the first to discover that pro-survival pathway activation is directly associated with p53-dependent genotoxic responses in cancer cells, and have provided a unique and significant contribution in this area. As an Assistant and then as an Associate Professor at the BIDMC and the MGH/Harvard Medical School, I pursued my major interest in how tumor suppressor p53-mediated transcriptional regulation influences cell fate decisions: live or die. Based on my contribution concerning the dark side of p53 in cancer therapeutics that wt-p53 can function as a guardian of cancer genome for their survival against therapeutic stress, I have established close collaborations with the Broad Institute utilizing their technological, computational and chemical biological tools under their Chemical Genetics Platform. Together with Broad scientists, I have identified several promising small molecules with anti-cancer activity through the activation of tumor suppressor p53 apoptotic pathway. Specifically, we have identified a small molecule to induce apoptosis selectively in cells having a cancer genotype by targeting a non-oncogene co-dependency acquired by the expression of the cancer genotype in response to transformation-induced oxidative stress. This highlights a novel strategy for cancer therapy that preferentially eradicates cancer cells by targeting the ROS stress-response pathway. My experience in this area has played a major role in the development of a Chemical Genetics Core facility at CBRC in collaboration with the Broad Institute. My group now possesses considerable experience in systematic small molecule technologies. I will continue to assist with the design, validation, execution and interpretation of investigator initiated chemical genetic screens.

Group Members

Kiki Chu

Aditi U Gurkar

Masatsugu Hiraki

So Young Hwang

Hyung Gu Kim

Lei Zheng

Chan Lee

Kyoung Wan Yoon

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617-522-3113

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