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Cancerous RAGE

Mounting evidence has linked chronic inflammation and cancer, but the sheer number of pathways and molecules that could be involved has slowed the identification of the molecular mechanisms that may lead inflamed tissue to become cancerous. Researchers at the German Cancer Research Center and Heidelberg University Hospital have found a molecular mechanism by which chronic inflammation promotes skin tumors in mice. The findings indicate that receptor for advanced glycosylation end products and its ligands could be a target in epithelial and possibly other cancers.

In the Jan. 21 online edition of The Journal of Experimental Medicine, a research team led by Peter Angel reported that feedback between NF-kB and receptor for advanced glycosylation end products (RAGE)-a cycle that sustains inflammation-activated tumor-promoting functions of two RAGE ligands, S100A8 and S100A9, and led to skin tumor growth in mice.1 Angel is head of the Division of Signal Transduction and Growth

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