Basic Biology of Aging: Nuclear and Mitochondrial mutagenesis: Theoretical and Clinical insights into cancer and aging

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Speaker

Jason Bielas, PhD
Affiliate Associate Professor
Department of Pathology
Fred Hutchinson Cancer Research Center


Date & Time

May 19, 2016 at 2:30pm - 3:30pm

Location

Foege N-130

Calendar

Basic Biology of Aging

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Add to Calendar 05/19/2016 02:30 PM 05/19/2016 03:30 PM America/Los_Angeles Basic Biology of Aging: Nuclear and Mitochondrial mutagenesis: Theoretical and Clinical insights into cancer and aging Basic Biology of Aging: Nuclear and Mitochondrial mutagenesis: Theoretical and Clinical insights into cancer and aging

Jason Bielas, PhD
Affiliate Associate Professor
Department of Pathology
Fred Hutchinson Cancer Research Center
Why Attend? Nuclear and Mitochondrial mutagenesis: Theoretical and Clinical insights into cancer and aging Mitochondrial mutations, some conferring pro-tumorigenic potential, are recur­rently identified in cancer, though how and why they arise is poorly understood. In the nucleus, clonal mutations may result from selection and expansion of de novo mutations arising from genetic instability. If this trend is recapitulated in mitochon­drial DNA (mtDNA), then mtDNA should display a mutator phenotype, i.e. frequent de novo mutations. However, we discovered decreased mtDNA rare point muta­tions in cancer compared to matched normal tissue. Influenced by these findings, we have re-examined the putative role of mitochondrial mutagenesis in cancer and aging, and highlight its potential as a therapeutic target for cancer treatment.
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Why Attend?

Nuclear and Mitochondrial mutagenesis: Theoretical and Clinical insights into cancer and aging

Mitochondrial mutations, some conferring pro-tumorigenic potential, are recur­rently identified in cancer, though how and why they arise is poorly understood. In the nucleus, clonal mutations may result from selection and expansion of de novo mutations arising from genetic instability. If this trend is recapitulated in mitochon­drial DNA (mtDNA), then mtDNA should display a mutator phenotype, i.e. frequent de novo mutations. However, we discovered decreased mtDNA rare point muta­tions in cancer compared to matched normal tissue. Influenced by these findings, we have re-examined the putative role of mitochondrial mutagenesis in cancer and aging, and highlight its potential as a therapeutic target for cancer treatment.