Peter S. Rabinovitch
Ph.D., University of Washington, Genetics, 1980.
M.D., University of Washington, Medicine, 1979.
The focus of the laboratory is upon studies of DNA damage and genomic instability in aging and in neoplastic progression. In aging, we are interested in the connection between DNA damage and free radical injury and 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 hat 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. 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 has proven to be one such a marker. In both aging and neoplasia, we are interested in the role of telomere shortening in promoting genomic instability. Additional molecular genetic and cytometric indicators of genomic instability and DNA repair are being studied.
Director, University of Washington Nathan Shock Center of Excellence in the Basic Biology of Aging
Director, University of Washington Genetic Approaches to Aging Training Grant
Director, Anatomic Pathology Flow Cytometry Laboratory, University of Washington Medical Center
International Society for Analytical Cytology
DNA Libraries (Methods for making and using single-chromosome amplification libraries, Patent Number: 5814444, , , United States of America.
Macrophage Mitochondrial Oxidative Stress Promotes Atherosclerosis and Nuclear Factor-κB-Mediated Inflammation in Macrophages.. Circulation research. 114(3):421-33.. 2014.
Response.. Journal of the National Cancer Institute. 106(2):djt437.. 2014.
Global proteomics and pathway analysis of pressure-overload-induced heart failure and its attenuation by mitochondrial-targeted peptides.. Circulation. Heart failure. 6(5):1067-76.. 2013.
Preserving youth: does rapamycin deliver? Science translational medicine. 5(211):211fs40.. 2013.
Clonal Expansions and Short Telomeres Are Associated with Neoplasia in Early-onset, but not Late-onset, Ulcerative Colitis.. Inflammatory bowel diseases. 19(12):2593-602.. 2013.
Independent and combined effects of dietary weight loss and exercise on leukocyte telomere length in postmenopausal women.. Obesity (Silver Spring, Md.).. 2013.
mTOR is a key modulator of ageing and age-related disease.. Nature. 493(7432):338-45.. 2013.
mTOR inhibition alleviates mitochondrial disease in a mouse model of Leigh syndrome.. Science (New York, N.Y.). 342(6165):1524-8.. 2013.
Mitochondria and tumor progression in ulcerative colitis.. Journal of the National Cancer Institute. 105(16):1239-48.. 2013.
A novel radial water tread maze tracks age-related cognitive decline in mice.. Pathobiology of aging & age related diseases. 3. 2013.
Topograph, a software platform for precursor enrichment corrected global protein turnover measurements.. Molecular & cellular proteomics : MCP.. 2012.
Ulcerative colitis-associated colorectal cancer arises in a field of short telomeres, senescence, and inflammation.. Cancer research. 71(5):1669-79.. 2011.
Genetic variation in prostaglandin E2 synthesis and signaling, prostaglandin dehydrogenase, and the risk of colorectal adenoma.. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 19(2):547-57.. 2010.
Array-based comparative genomic hybridization in ulcerative colitis neoplasia: single non-dysplastic biopsies distinguish progressors from non-progressors.. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc. 23(12):1624-33.. 2010.
Deletion at fragile sites is a common and early event in Barrett's esophagus.. Molecular cancer research : MCR. 8(8):1084-94.. 2010.
Polyploidy, aneuploidy and the evolution of cancer.. Advances in experimental medicine and biology. 676:1-13.. 2010.
Proteins That Underlie Neoplastic Progression of Ulcerative Colitis.. Proteomics. Clinical applications. 3(11):1326-1337.. 2009.
Nonadenomatous dysplasia in barrett esophagus: a clinical, pathologic, and DNA content flow cytometric study.. The American journal of surgical pathology. 33(6):886-93.. 2009.
No telomere shortening in marrow stroma from patients with MDS.. Annals of hematology. 88(7):623-8.. 2009.
Clonal expansions in ulcerative colitis identify patients with neoplasia.. Proceedings of the National Academy of Sciences of the United States of America. 106(49):20871-6.. 2009.
Cell proliferation, cell cycle abnormalities, and cancer outcome in patients with Barrett's esophagus: a long-term prospective study.. Clinical cancer research : an official journal of the American Association for Cancer Research. 14(21):6988-95.. 2008.
Reduction of age-associated pathology in old mice by overexpression of catalase in mitochondria.. The journals of gerontology. Series A, Biological sciences and medical sciences. 63(8):813-22.. 2008.
Ulcerative colitis is a disease of accelerated colon aging: evidence from telomere attrition and DNA damage.. Gastroenterology. 135(2):410-8.. 2008.
Dietary supplement use and risk of neoplastic progression in esophageal adenocarcinoma: a prospective study.. Nutrition and cancer. 60(1):39-48.. 2008.