The findings are the first fruit of an approach that seeks a systematic route to the development of new cancer therapies. By scanning the DNA of cancer cells, Dana Farber scientists and colleagues at the Massachusetts Institute of Technology's Broad Institute are hunting for mutated genes that instruct cells to produce abnormal versions of growth proteins called tyrosine kinases. The hope is that drugs known to block such proteins can stymie cancer growth while leaving normal cells intact.

The study will be published this week in the online version of the journal Science (www.sciencemag.org). Related research from Massachusetts General Hospital Cancer Center, a member of the Dana-Farber/Harvard Cancer Center, will be concurrently released online by the New England Journal of Medicine on April 29.

"Imatinib (GleevecTM) [which has halted or shrunk tumors in patients with a form of leukemia and digestive-system tumor] is probably the best-known example of a drug that works by targeting a specific, mutated tyrosine kinase," says William Sellers, M.D., who is co-senior author of the study with his Dana-Farber colleagues Bruce Johnson, M.D., and Matthew Meyerson, M.D., Ph.D. "So far, though, this approach has been most notable in cancers that are relatively rare. Our study shows that it can be effective for a common form of cancer as well." Non-small cell lung cancer (NSCLC) accounts for about 85 percent of all cases of lung cancer, the number one cancer killer of both men and women in the United States.

The study's lead authors are J. Guillermo Paez, Ph.D., and Pasi Janne, M
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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
29-Apr-2004