Abstract
Helicobacter pylori is one of the primary reasons that the gastric epithelium becomes chronically inflamed. As with other epithelial tissues, chronic inflammation can lead to hyperproliferation, metaplasia and eventually gastric cancer. The hedgehog (Hh) pathway is required for embryonic development including development of the gastrointestinal tract. In the pancreas, Hh signaling is extinguished after birth but becomes re-activated by chronic inflammation and when sustained contributes to pancreatic cancer. However, the contribution of Hh signaling in gastric cancer has been less clear. Components of the Hh pathway are elevated in human gastric cancer cell lines, and on this basis, its contribution to gastric cancers have been implicated. Unlike the pancreas, the gastric corpus produces abundant amounts of the Sonic Hedgehog (Shh) ligand. Recent studies have indicated that Shh expressed in the acid-producing parietal cells is required to recruit myeloid cells to the stomach during the initial phase of a Helicobacter infection. We will present evidence showing that the canonical Hh target gene Gli1 is required for the Helicobacter-induced inflammatory response as well as the subsequent development of mucous cell metaplasia, a pre-neoplastic lesion in the stomach.
Citation Format: Juanita L. Merchant. Helicobacter gastritis, metaplasia, and gastric cancer. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr PL02-02.
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