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Anthony G. Letai, MD, PhD


Medical Oncology

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Physician

  • Physician
  • Associate Professor of Medicine, Harvard Medical School

Centers/Programs

Clinical Interests

  • Leukemias

Contact Information

  • Appointments617-632-6140
  • Office Phone Number617-632-2348
  • Fax617-582-8160

Bio

Dr. Letai received his MD and PhD from the University of Chicago. He completed his residency in internal medicine at Brigham and Women's Hospital, and a fellowship in hematology and oncology at DFCI. He did his postdoctoral research training in the laboratory of Dr. Stanley Korsmeyer. Dr. Letai's research focuses on the mechanisms by which cancer cells evade death, and on the application of that knowledge to the selective killing of cancer cells. He joined the faculty of DFCI and Harvard Medical School in 2004.

Board Certification:

  • Medical Oncology, 2001

Fellowship:

  • Dana-Farber/Partners CancerCare, Hematology/Oncology

Residency:

  • Brigham and Women's Hospital, Internal Medicine

Medical School:

  • University of Chicago

Recent Awards:

  • Leukemia and Lymphoma Society Scholar Award 2008
  • American Society of Clinical Investigation, Elected Member 2009
  • V Scholar Award 2005
  • Smith Family New Investigator 2004
  • Kimmel Scholar Award 2005

Location

Dana-Farber Cancer Institute
450 Brookline Avenue
Mayer 429
Boston MA, 02215
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Research

Dysregulation of Death Pathways in Cancer

The cells of the body are constructed so that if they become sufficiently damaged or abnormal, programmed cell death, or apoptosis, rapidly eliminates them before they can cause any harm. Cancer cells, which bear many abnormalities, apparently have found ways to escape this death sentence. One way that cancer cells escape death is via the overexpression of antideath proteins in the BCL-2 family. We are investigating how these antideath proteins might be selectively targeted in cancer cells.

Using a combination of mouse models, protein biochemistry, and mitochondrial and cellular studies, we have determined conditions under which cancer and normal cells are susceptible to inhibition of BCL-2 family function. We are collaborating with biotechnology and pharmaceutical firms to bring small-molecule BCL-2 antagonists to clinical trial here at Dana-Farber. Most likely, the novel strategy of BCL-2 antagonism will first be tested in chronic lymphocytic leukemia, small-cell lung cancer, and non-Hodgkin's lymphoma. If these trials are successful, the strategy of BCL-2 antagonism may find wide application in other human cancers.

We also investigate more fundamental questions about how interactions among BCL-2 family proteins govern death and survival in normal and cancer cells. We explore how these proteins participate in a wide range of death signals, growth factor withdrawal, and chemotherapy.

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