Helicobacter pylori cagA+ strains cause gastric inflammation, ulcers, and cancer. Previous reports have shown that the cagA gene-encoded protein “CagA” plays a crucial role in gastric carcinogenesis. However, the underlying mechanisms remain to be fully elucidated. Researchers from Japan used animal models and laboratory-cultured human gastric epithelial cells to demonstrate that CagA works by disrupting the Wnt/Planar Cell Polarity (PCP) signaling pathway.
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