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UB researchers show first evidence of pharmacogenomic differences in patients' responses to MS drug

BUFFALO, N.Y. - University at Buffalo researchers using the latest computer-assisted technologies of genetic analysis have shown for the first time how a widely used drug for treating multiple sclerosis -- interferon beta (IFN-beta-1a) -- can modulate the expression of particular genes in patients being treated for the disease.

Their results show that IFN-beta-1a initiates different patterns of genetic expression in different MS patients, information that could lead to better, and potentially individualized, treatments.

Results of the study were presented Oct. 21 at the annual meeting of the American Neurological Association in San Francisco by Bianca Weinstock-Guttman, M.D., UB assistant professor of neurology and director of the Baird MS Center at The Jacobs Neurological Institute, the research arm of the UB Department of Neurology. The study also appeared in the September issue of The Journal of Immunology.

The work links gene microarray techniques with the science of pharmacogenomics and pharmacodynamics. Microarrays are tools for measuring the expression of large numbers of genes. Pharmacodynamics uses mathematical models to capture the details of how drugs affect the body's systems over time, starting with the moment of exposure to the drug.

Together, these techniques can be used to find how genes interact with each other and how a cell's regulatory networks control vast batteries of genes simultaneously. Murali Ramanathan, Ph.D., UB associate professor of pharmaceutical sciences, who performed the experimental assays, has broad experience in processing and analyzing this complex information.

"In a small group of patients, we found that the mRNA gene expression in response to IFN-beta-1a increased rapidly in some MS patients, and was low and late in other patients," said Weinstock-Guttman. "We were very surprised that some of the gene markers showed up as early as two hours after we administered the drug. Prior to this work, oth
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Contact: Lois Baker
ljbaker@buffalo.edu
716-645-5000 x1417
University at Buffalo
28-Oct-2003


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