We show for the first time that CagA(+) H. pylori upregulates cellular invasiveness and motility through casein kinase 2. The demonstration of a mechanistic interplay between H. pylori and casein kinase 2 provides important insights into the role of CagA(+) H. pylori in the gastric cancer invasion and metastasis.
For neoplasms with undifferentiated histology (PD or SRC), short-term endoscopic follow-up may help to detect residual tumors that form after complete resection via ER. For EGC, the lateral margin may be considered safe if greater than 3 mm. However, the possibility of satellite lesions should be investigated when the gastric adenoma to be resected is surrounded by severe IM.
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