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职业迁徙
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My laboratory team examines aspects of DNA repair and carcinogenesis, focusing on two major pathways that have been implicated in cancer development: mismatch repair (MMR) and homologous recombination (HR). We were the first to show that the human MMR genes MSH2 and MLH1 were the cause of the common cancer predisposition known as Lynch syndrome, or hereditary non-polyposis colorectal cancer (LS/HNPCC). This work provided a fundamental foundation for the now-widespread concept that genome instability is a major driver of tumorigenesis.
In recent years, my lab has developed multiple real-time single-molecule imaging instruments that have contributed to entirely new methods for the quantitative mechanical analysis of MMR and HR in vivo and in vitro. These studies have led to innovative mechanisms that have overturned decades of dogma in the DNA repair field. In addition, we have established preclinical models for LS/HNPCC that have led to non-steroidal anti-inflammatory (NSAID) compounds, such as aspirin and naproxen, to be utilized as chemoprevention strategies, which are currently a standard of care or in clinical trials.
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Michael A. Mcilhatton,Jessica Tyler, Laura A. Kerepesi, Tina Bocker-Edmonston,Melanie H. Kucherlapati,Winfried Edelmann,Raju Kucherlapati,Levy Kopelovich,Richard Fishel
crossref(2023)
Nature Communicationsno. 1 (2022): 5808-17
Journal of Biological Chemistryno. 11 (2022): 102505-102505
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