Mitchell Turker, Ph.D., J.D.
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- Phone:
- 503 494-2168
Background
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 Activities I 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.
Selected Publications
"Hypoxia-induced epigenetic regulation and silencing of the BRCA1 promoter,"
"Marked aneuploidy and loss of multiple chromosomes are common in autosomal mutants isolated from normal mouse kidney epithelium,"
"Aberrantly silenced promoters retain a persistent memory of the silenced state after long-term reactivation,"
"In Utero Life and Epigenetic Predisposition for Disease,"
"Erratum: Comparison of autosomal mutations in mouse kidney epithelial cells exposed to iron ions in situ or in culture. (Radiation Research (2009) 172 (558-566)),"
