Infection with Helicobacter pylori is linked to a wide range of gastric disorders, including stomach cancer. Although only a small proportion of infected individuals develop cancer, most cases of gastric cancer are attributed to H. pylori. Several virulence factors have been implicated in H. pylori-associated carcinogenesis, particularly the effector protein CagA. Here, Neal and colleagues use a novel transgenic zebrafish model to investigate the effects of CagA on digestive tract epithelial cells. They demonstrate that CagA induces proliferation of the zebrafish intestinal epithelium via activation of the canonical Wnt signalling pathway. In addition, they provide the first in vivo evidence for cooperation between CagA and the tumour suppressor p53 in oncogenesis. The study highlights the potential of the zebrafish system for exploring genetic interactions between pathogen virulence effectors and host cell signalling proteins. Page 802
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IN THIS ISSUE| 01 May 2013
Role of CagA in H. pylori gastric cancer
Online Issn: 1754-8411
Print Issn: 1754-8403
Written by editorial staff. © 2013. Published by The Company of Biologists Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
Dis Model Mech (2013) 6 (3): 555–556.
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Role of CagA in H. pylori gastric cancer. Dis Model Mech 1 May 2013; 6 (3): 555–556. doi:
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