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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