Peter Rabinovitch, MD, PhD

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Dr. Peter Rabinovich MD, PhD
faculty member

Peter Rabinovitch, MD, PhD

Professor, Public Health Sciences Division, Fred Hutch

Professor
Public Health Sciences Division, Fred Hutch

Fax: 206.667.5530
Mail Stop: C1-157

Dr. Peter Rabinovitch studies cellular damage and genomic instability (i.e., high frequency of genetic mutations) in aging and cancer progression. In aging, his team uses mouse models to explore the connection between DNA damage, free-radical injury, mitochondrial function, lifespan and disease. His studies of cancer progression focus on human gastrointestinal cancers and precancerous diseases such as ulcerative colitis. Better understanding these diseases’ progression may yield biomarkers that could indicate which patients with precancerous conditions are at increased risk of going on to develop cancer.

Other Appointments & Affiliations

Professor, Pathology, University of Washington School of Medicine

Professor, Pathology
University of Washington School of Medicine

Education

PhD, Genetics, University of Washington, 1980

MD, University of Washington, 1979

Research Interests

In aging, his team is interested in the connection between DNA damage, free-radical injury, mitochondrial energy supply, lifespan and disease. Transgenic mice that overexpress antioxidant enzymes have enhanced longevity and are being examined to provide insights in this model system. In particular, mice that overexpress catalase targeted to mitochondria have extended longevity and healthspan — the latter includes resistance to cardiac aging and experimental heart disease, reduced sarcopenia, and resistance to non-hematological malignancies. Dr. Rabinovitch is studying pharmacologic agents that similarly impact mitochondrial biology, including the cardiolipin targeted drug elamipretide (A.K.A. SS-31), which appears to confer many of the same beneficial effects.

Studies of neoplastic progression focus on human gastrointestinal cancers and precancerous diseases such as ulcerative colitis. A better understanding of neoplastic progression in these diseases may yield biomarkers of increased clinical risk for progression to cancer. Genomic instability, as identified by flow cytometry and telomere length measurements have been found to have promise as such markers. Additional molecular genetic indicators of genomic instability and DNA repair are now being studied.

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