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Upcoming Distinguished Lecturer Stephen West

By Eddy Ball
April 2010

Stephen West, Ph.D.
After completing a postdoctoral fellowship and serving as a research scientist in the Department of Therapeutic Radiology at Yale University, West returned to his native England in 1989. (Photo courtesy of Stephen West)

The NIEHS Distinguished Lecture Series highlights the links between mutagenesis and cancer with a talk on April 13 by Stephen West, Ph.D. Hosted by Laboratory of Molecular Genetics Staff Scientist Dmitry Gordenin, Ph.D., West's lecture will explore "Defective DNA Strand Break Repair and Links to Inheritable Disease."

West( Exit NIEHS is currently the associate director of Clare Hall Laboratories, a division of the Cancer Research United Kingdom London Research Institute (LRI), and senior group leader of the Genetic Recombination Laboratory there. In 1995, West was elected a fellow of the Royal Society. He has also received several other prestigious awards for his work, including the Swiss Bridge Prize Award for Cancer Research in 2001 and again in 2009, the Louis-Jeantet Prize for Medicine in 2007, and the Novartis medal and prize from the Biochemical Society in 2008.

The West Group specializes in basic research into mechanisms of DNA replication, recombination, repair, and cell cycle, exploring the relationships between genome instability and cancer. The group is recognized for its research into the genome instability associated with mutations in the BRCA genes, which is caused by defective recombination processes and appears to underlie certain inheritable breast and ovarian cancers. According to West, approximately 20 percent of breast cancers are inheritable, and of those about one-third have been linked to mutations in BRCA1 or BRCA2.

West has also made important discoveries about loss of activity of the protein Aprataxin, which plays a critically important cellular role in guarding the genome against DNA damages that would otherwise pose a block to normal cellular processes. His group defined this molecular defect and its role in the neurological disorder known as Ataxia with Oculomotor Apraxia-1 (AOA1).

In 2008, the West Group identified a key enzyme in mammals, ResA, which is involved in the process of homologous recombination - one of the ways an organism repairs breaks in its DNA. A defect in the production of this specialized enzyme, one of what are called the Holliday junction resolvases, short-circuits the proper chromosome segregation necessary for DNA repair.

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