PurposeAdditional surgery is commonly recommended in gastric cancer patients who have a high risk of lymph node metastasis or a positive resection margin after endoscopic resection. We conducted this study to determine factors related to residual cancer and to determine the appropriate treatment strategy.Materials and MethodsA total of 28 patients who underwent curative gastrectomy due to non-curative endoscopic resection for early gastric cancer between January 2006 and June 2009 were enrolled in this study. Their clinicopathological findings were reviewed retrospectively and analyzed for residual cancer.ResultsOf the 28 patients, surgical specimens showed residual cancers in eight cases (28.6%) and lymph node metastasis in one case (3.8%). Based on results of the endoscopic resection method, the rate of residual cancer was significantly different between the en-bloc resection group (17.4%) and the piecemeal resection group (80.0%). The rate of residual cancer was significantly different between the diffuse type group (100%) and the intestinal type group (20%). The rate of residual cancer in the positive lateral margin group (25.0%) was significantly lower than that in the positive vertical margin group (33.3%) or in the positive lateral and vertical margin group (66.7%).ConclusionsWe recommended that patients who were lateral and vertical margin positive, had a diffuse type, or underwent piecemeal endoscopic resection, should be treated by surgery. Minimal invasive procedures can be considered for patients who were lateral margin positive and intestinal type through histopathological examination after en-bloc endoscopic resection.
Rebamipide a gastroprotective drug, is clinically used for the treatment of gastric ulcers and gastritis, but its actions on gastric cancer are not clearly understood. Phospholipase D (PLD) is overexpressed in various types of cancer tissues and has been implicated as a critical factor in inflammation and carcinogenesis. However, whether rebamipide is involved in the regulation of PLD in gastric cancer cells is not known. In this study, we showed that rebamipide significantly suppressed the expression of both PLD1 and PLD2 at a transcriptional level in AGS and MKN-1 gastric cancer cells. Downregulation of PLD expression by rebamipide inhibited its enzymatic activity. In addition, rebamipide inhibited the transactivation of nuclear factor kappa B (NFκB), which increased PLD1 expression. Rebamipide or PLD knockdown significantly suppressed the expression of genes involved in inflammation and proliferation and inhibited the proliferation of gastric cancer cells. In conclusion, rebamipide-induced downregulation of PLD may contribute to the inhibition of inflammation and proliferation in gastric cancer.
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