
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Special Section |
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California
Requests for reprints: Anne Mueller, Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305-5124. Phone: 650-723-2671; Fax: 650-723-1837. E-mail: muellera{at}stanford.edu
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.
This article has been cited by other articles:
![]() |
S K Tiwari, G Manoj, G V. Kumar, G Sivaram, S I Hassan, B Prabhakar, U Devi, S Jalaluddin, K Kumar, S Ahmed, et al. Prognostic significance of genotyping Helicobacter pylori infection in patients in younger age groups with gastric cancer Postgrad. Med. J., April 1, 2008; 84(990): 193 - 197. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Cell Growth & Differentiation |