Discovery of gene will likely lead to new treatments for inflammatory diseases, cancer

(Boston) -- In a paper featured today in Proceedings of the National Academy of Science (PNAS), researchers from Boston University School of Dental Medicine report the discovery of a new gene, STAT6(B), that helps regulate production of the potentially deadly tumor necrosis factor alpha (TNF-alpha) cytokine. TNF-alpha is involved in inflammatory disorders such as Crohn's disease, rheumatoid arthritis, and irritable bowel syndrome. The paper is the first by a dental school researcher to be chosen as a featured article in PNAS.

The new gene also regulates vascular endothelial growth factor (VEGF), which is responsible for new blood vessels. Blocking excess amounts of VEGF has already led to the cancer therapeutic Avastin; STAT6(B) works through a different mechanism and thus will offer new opportunities for treating cancer. The researchers are publishing this finding in a separate paper.

STAT6(B), which is similar to the previously known STAT6 gene, works closely with a gene known as LITAF, discovered by the same Boston University researchers in 1999. The STAT6(B) and LITAF proteins (which are coded for by their respective genes) bind to form a complex that moves into the cell's nucleus to regulate the transcription of cytokines. The recent Boston University findings will offer new ways to regulate TNF-alpha, whose overexpression causes inflammatory and immunological problems.

Drugs regulating TNF-alpha such as Remicade, Embrel, and Humira are a multibillion dollar market. "Because STAT6(B) and LITAF affect TNF-alpha through a different pathway, we expect to develop more efficient therapeutics to help people with rheumatoid arthritis, Crohn's disease, and inflammatory bowel syndrome," says Boston University School of Dental Medicine Professor Salomon Amar, the leading author of the paper.

The Boston University researchers are now working on animal models to control LITAF and thus TNF-alpha overproduction in inflammatory syndromes. <

Contact: Mari Megias
Boston University

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