Mitchell Turker, Ph.D., J.D.
Dr. Turker received his PhD in Pathology from the University of Washington (UW) and was a post-doctoral fellow at the University of Colorado Health Sciences Center. He served as a Research Instructor in the Department of Pathology at UW. He went on to the University of Kentucky where he served as an Assistant Professor and Associate Professor in the Departments of Pathology and Microbiology/Immunology and Director, Experimental Pathology. Prior to joining CROET, he was a visiting Associate Professor in the Department of Genetics and Development at Columbia University.Research ActivitiesI am interested in the mechanisms of abnormal gene inactivation and the relevance of these events to cancer and aging. Cancer and aging are linked because the incidence of cancer increases as we get older, but the reasons for this link are not understood. One possible mechanism that can explain this link is aberrant gene inactivation, because it is known that gene inactivation plays a critical role in cancer, and it is believed that the frequency of gene inactivation increases as a function of age. Abnormal gene inactivation results from two distinct types of events. The first is DNA mutation, which represents a change in the structure of DNA that alters expression of a given gene. The second type of event is DNA methylation, which causes silencing of a gene without affecting the gene sequence. My laboratory is using the autosomal mouse Aprt gene to study both mutational and DNA methylation events. With regard to mutational events, we are interested in both endogenous and exogenous genotoxins that can affect the frequency and types of mutations that occur within the animal. Our work with DNA methylation focuses on how methylation patterns are formed and on how perturbations of these patterns can lead to silencing of genes.
"Autosomal mutants of proton-exposed kidney cells display frequent loss of heterozygosity on nonselected chromosomes,"
"Silencing of the DNA Mismatch Repair Gene MLH1 Induced by Hypoxic Stress in a Pathway Dependent on the Histone Demethylase LSD1,"
"Autosomal mutations in mouse kidney epithelial cells exposed to high-energy protons in vivo or in culture,"
"Comparative analysis of cell killing and autosomal mutation in mouse kidney epithelium exposed to 1 GeV protons in vitro or in vivo,"
"Epigenetic patents: A stressful environment for an emerging science,"