Abstract

Abstract Aim: Although minimal invasive treatment is widely accepted for early stage of gastric cancer, we still do not have any appropriate risk markers to detect residual neoplasia and some potential of recurrence. We previously reported that aberrant DNA methylation is an early and frequent process in gastric carcinogenesis and could be useful for detection of gastric neoplasia, and that methylation analysis of DNA recovered from gastric washes was used to detect gastric neoplasia (Gastroenterology 2009). Here, we hypothesized gastric washes also can determine whether gastric cancer (GCa) was removed curatively by endoscopic treatment or not. Our goal is to find and identify some candidate genes as a treatment marker using genome wide DNA methylation analysis and for early gastric cancer. Method: We studied MCAM (Methylated CpG Island Amplification Microarray) analysis using 12 gastric washes (each 6 before and after endoscopic treatment in same patients) and identified candidate genes for further studies. Two of them are MINT25 and Sox17 (SRY (sex determining region Y)-box 17). We examined the DNA methylation status of these two genes in a validation set consisting of 128 washes samples (Pre, 64: Post, 64) at early gastric cancers by quantitative bisulfite-pyrosequencing analysis. Results: These two genes showed significantly differential methylation between before and after treatment in GCa patient (MINT25, p<0.0001: Sox17, p<0.0001). Moreover, we could successfully identified the incomplete endoscopic mucosal resection case by Sox17 methylation status, and additional resection resulted in the proof of residual cancer and decrease of Sox17 methylation level in gastric wash. Conclusion: We have developed a new methodology for gastric cancer detection by DNA methylation in gastric washes. It is easy and useful for early detection of recurrence after endoscopic treatment in GCa patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 93. doi:10.1158/1538-7445.AM2011-93

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