Sam W. Lee

Boston , Masschusetts

Sam W. Lee, PHD, completed his doctoral studies at the University of California-Berkeley in 1988. Following that, he worked at the University of California-San Francisco as a post-doctorate fellow. Sam W. Lee served as an assistant professor at the University of Michigan Medical School in the Division of Cancer Biology.

Sam W. Lee first worked with the Harvard College medical school in 1989 and has maintained a working relationship since then.

Most of Lee’s work has come in research. Lee has published over 100 papers. Lee’s most significant contribution came as an independent investigator in the field of p53 down stream targets involved in apoptosis and survival. He was the first to discover that pro-survival pathway activation is directly associated with p53-dependent DNA damage/geno-toxic responses in cancer cells, and have provided a unique and very significant contribution in this area.

Sam W. Lee completed Ph.D. in Molecular Genetics under Dr. Agabian at University of California. He trained as a postdoctoral fellow in the laboratories of Ruth Sager at the Dana Farber Cancer Institute/Harvard Medical School, where he began his studies on the transcriptional regulation of breast cancer genes. As an Assistant and then as an Associate Professor at the BIDMC and the MGH/Harvard Medical School, Lee pursued his major interest in how tumor suppressor p53-mediated transcriptional regulation influences cell fate decisions: live or die.

Anti-cancer therapies, including radiation and chemotherapeutic agents, ultimately eliminate tumor cells by the induction of apoptosis. However, this therapeutic opportunity is eroded by pro-survival mechanisms that inhibit apoptosis. This is expected to promote selective death of tumor cells or to sensitize tumor cells to therapy-induced apoptosis.

Sam W. Lee has been serving the NIH study section as a panel member for the last 10 years. Since 2010, Sam W. Lee has become an associate member of the Broad Institute of Harvard/MIT. His group has identified several promising small molecules with anti-cancer activity through the activation of tumor suppressor p53 apoptotic pathway. Sam W. Lee’s group now possesses considerable experience in systematic small molecule technologies. These efforts to promote awareness and usage among MGH scientists of the chemical genetics platforms established at the Broad Institute were able to bring individual investigators within the academic communit

  • Work
    • Research assistant with Broad Institute
  • Education
    • University of California Berkeley