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Cancer Cell. 2008 Jul 8;14(1):7-9. doi: 10.1016/j.ccr.2008.06.010.

Inflaming gastrointestinal oncogenic programming.

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Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.


The etiology of gastrointestinal tumors implicates a role for chronic inflammation in response to pathogenic microflora as a promoting force for full neoplastic progression. Recently, Oguma and coworkers (2008) demonstrated that TNFalpha, derived from recruited macrophages, potentiates Wnt/beta-catenin signaling and gastric carcinogenesis by activating Akt signaling and GSK3beta phosphorylation independent of the NF-kappaB pathway in initiated epithelial cells. These observations provide a missing link in the mechanism whereby chronic inflammation, in response to Helicobacter, regulates the "penetrance" of initiating oncogenic mutations in the gastrointestinal tract leading to gastrointestinal tumorigenesis.

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