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Publication : Inflaming gastrointestinal oncogenic programming.

First Author  DeNardo DG Year  2008
Journal  Cancer Cell Volume  14
Issue  1 Pages  7-9
PubMed ID  18598939 Mgi Jnum  J:138702
Mgi Id  MGI:3806178 Doi  10.1016/j.ccr.2008.06.010
Citation  DeNardo DG, et al. (2008) Inflaming gastrointestinal oncogenic programming. Cancer Cell 14(1):7-9
abstractText  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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