Helicobacter pylori and gastric cancer: what can be learned by studying the response of gastric epithelial cells to the infection?
The development of gastric adenocarcinoma is closely linked to chronic infection with the bacterial pathogen Helicobacter pylori. One Helicobacter-specific virulence factor in particular, the CagA protein, has emerged as a main effector molecule in the interaction of H. pylori with gastric epithelial cells and has been implicated in gastric carcinogenesis. This review highlights the latest insights that have been gained into the pathogenesis of the disease by transcriptional profiling approaches studying gene expression in normal gastric tissue and gastric cancer tissue from human biopsy material as well as animal models of Helicobacter infection. The potential role of CagA as a bacterial oncoprotein is also discussed.
Mueller
Anne
A
Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305-5124, USA. muellera@stanford.edu
Falkow
Stanley
S
Amieva
Manuel R
MR
D000230:Adenocarcinoma / Q000209:etiology / Q000382:microbiology / Q000473:pathology; D000818:Animals; D000942:Antigens, Bacterial / Q000235:genetics / Q000502:physiology*; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D013274:Stomach Neoplasms / Q000209:etiology / Q000382:microbiology / Q000473:pathology
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori