Dr. Michele K. Evans, a board certified internist and medical oncologist, received her medical degree from the University of Medicine and Dentistry of New Jersey-The Robert Wood Johnson Medical School in Piscataway. She received her postgraduate training in internal medicine at Emory University School of Medicine and fellowship training in medical oncology within the Medicine Branch of the Clinical Oncology Program at the National Cancer Institute (NCI). Interest in human cancer prone disorders and DNA repair led her to study the role of DNA repair in cancer susceptibility as a Senior Clinical Investigator in the Laboratory of Molecular Pharmacology, NCI. At the National Institute on Aging (NIA), her major research interest centers on the clinical implications of eukaryotic DNA repair in cancer pathogenesis and aging. She also conducts epidemiologic work in the area of health disparities. Dr. Evans also serves as Deputy Scientific Director, NIA.
Powe CE, Evans MK, Wenger J, Zonderman AB, Berg AH, Nalls M, Tamez H, Zhang D, Bhan I, Karumanchi SA, Powe NR, Thadhani R. Vitamin D-binding protein and vitamin D status of black Americans and white Americans.N Engl J Med. 2013;369(21):1991-2000.
Noren Hooten N, Ejiogu N, Zonderman AB, Evans MK. Association of oxidative DNA damage and C-reactive protein in women at risk for cardiovascular disease. Arterioscler Thromb Vasc Biol. 2012;32(11):2776-84.
Kim Y, Noren Hooten N, Dluzen DF, Martindale JL, Gorospe M, Evans MK. Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637. Mol Cell Biol. 2015;35(24):4212-21.
Zonderman AB, Mode NA, Ejiogu N, Evans MK. Race and Poverty Status as a Risk for Overall Mortality in Community-Dwelling Middle-Aged Adults. JAMA Intern Med. 2016;176(9):1394-5.
DNA repair mechanisms are believed to play a vital role in the maintenance of genome integrity. Loss of fidelity in the replicative mechanism, accumulation of genetic lesions, and faulty DNA repair mechanisms facilitate tumorigenesis. Similarly, aging or cellular senescence is characterized by random accumulation of damage or mutation in DNA, RNA, or proteins and perhaps a diminished ability to repair DNA. The increased incidence of cancer as a function of age underscores the mechanistic relatedness of these two cellular processes. The diminished ability to repair DNA appears to be the crucial and convergent factor highlighting the important clinical manifestations associated with defects in DNA repair mechanisms. The overall thrust of our work has been to understand the role of DNA repair in cellular senescence and tumorigenesis in order to uncover ways to use measured DNA repair capacity as a clinical tool in the diagnosis and treatment of cancer and age-related disease and disability.