Abstract

BackgroundEarly detection of remnant gastric cancer (RGC) is required to reduce the risk of death, but long-term endoscopic surveillance is difficult after gastrectomy. In this study, data for the methylation status of 4 methylation genes (CDO1, HOPX, Reprimo, and E-cadherin) to predict the onset of RGC are presented.ResultsThe 4 genes showed hypermethylation in RGC tumors in contrast to the corresponding non-cancerous mucosa tissues. The methylation level in the non-cancerous mucosa tissues of the initial surgery was obviously high in initial malignant disease for CDO1 (P = 0.0001), while in initial benign one for E-cadherin (P = 0.003). Promoter DNA methylation status in the remnant non-cancerous mucosa tissues together with the basic clinical data in turn predicted either initial malignant disease or initial benign disease with a high AUC score of 0.94, suggesting that methylation events are differentially recognized between the initial malignant and benign disease. We then finally confirmed that 4 genes hypermethylation of the non-cancerous tissues by biopsy prior to onset of RGC could predict terms until RGC occurred (P < 0.0001).MethodsA total of 58 RGC patients were used to establish the model. The 4 genes promoter methylation were analyzed for DNA obtained from the patient’s specimens using quantitative methylation specific polymerase chain reaction.ConclusionsThis risk model would help provide guidance for endoscopic surveillance plan of RGC after gastrectomy.

Highlights

  • Remnant gastric cancer (RGC) arises in the remnant stomach after gastrectomy [1]

  • The methylation level in the noncancerous mucosa tissues of the initial surgery was obviously high in initial malignant disease for cysteine dioxygenase 1 (CDO1) (P = 0.0001), while in initial benign one for E-cadherin (P = 0.003)

  • The most outstanding clinicopathological characteristic was the term from the initial operation to onset of remnant gastric cancer (RGC), which was significantly shorter in patients with malignant disease (191.5 ± 127.5 months) than in those with benign disease (485.7 ± 86.7 months; P < 0.0001)

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Summary

Introduction

Remnant gastric cancer (RGC) arises in the remnant stomach after gastrectomy [1]. The development of RGC has been considered to be influenced by extrinsic factors such as decreased motor function and bile reflux [2,3,4,5]. Billroth II reconstruction has been reported to carry an increased risk of RGC because of bile reflux [6]. Other intrinsic factors including Helicobacter pylori (HP) infection [7], Epstein-Barr virus infection [8], and microsatellite instability [9] are implicated in the development of RGC. Markers to predict the risk of RGC are highly demanded. Detection of remnant gastric cancer (RGC) is required to reduce the risk of death, but long-term endoscopic surveillance is difficult after gastrectomy. Data for the methylation status of 4 methylation genes (CDO1, HOPX, Reprimo, and E-cadherin) to predict the onset of RGC are presented

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