Superficial non-ampullary duodenal epithelial tumor (SNADET) is defined as a sporadic tumor that is confined to the mucosa or submucosa that does not arise from Vater's papilla, and it includes adenoma and adenocarcinoma. Recent developments in endoscopic technology, such as high-resolution endoscopy and image-enhanced endoscopy, may increase the chances of detecting SNADET lesions. However, because SNADET is rare, little is known about its preoperative endoscopic diagnosis. The use of endoscopic resection for SNADET, which has no risk of metastasis, is increasing, but the incidence of complications, such as perforation, is significantly higher than in any other part of the digestive tract. A preoperative diagnosis is required to distinguish between lesions that should be followed up and those that require treatment. Retrospective studies have revealed certain endoscopic findings that suggest malignancy. In recent years, several new imaging modalities have been developed and explored for real-time diagnosis of these lesion types. Establishing an endoscopic diagnostic tool to differentiate between adenoma and adenocarcinoma in SNADET lesions is required to select the most appropriate treatment. This review describes the current state of knowledge about preoperative endoscopic diagnosis of SNADETs, such as duodenal adenoma and duodenal adenocarcinoma. Newer endoscopic techniques, including magnifying endoscopy, may help to guide these diagnostics, but their additional advantages remain unclear, and further studies are required to clarify these issues.

Background and study aims: Although magnifying endoscopy with narrow-band imaging (M-NBI) is useful for the diagnosis of gastric mucosal lesions, differentiating between early cancer (EC) and low grade adenoma (LGA) remains a challenge. During M-NBI examination, we have noted the presence of a small, white lesion with a globular shape underneath cancerous gastric epithelium, and have termed this endoscopic finding the “white globe appearance” (WGA). The aim of this study was to determine whether or not the WGA could be an endoscopic marker for distinguishing EC from LGA. Methods: We retrospectively analyzed both the M-NBI scans and resected specimens of a total of 111 gastric lesions from 95 consecutive patients. Our main outcome was a difference in the prevalence of the WGA in EC and LGA. Results: The prevalence of the WGA in EC and LGA was 21.5 % (20 /93) and 0 % (0 /18), respectively (P = 0.039). The sensitivity, specificity, positive predictive value, and negative predictive value for differentiating between EC and LGA, according to the presence of the WGA, were 21.5, 100, 100, and 19.8 %, respectively. Conclusion: A positive WGA in a suspicious lesion on M-NBI would be an adjunct to the M-NBI diagnosis of possible EC because the specificity and positive predictive value of the WGA for differentiating between EC and LGA were extremely high. The WGA could be a novel endoscopic marker for differentiating between EC and LGA.

The CSM with PLT was effective and safe in this study.

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The molecular and clinical characteristics of non-ampullary duodenal adenomas and intramucosal adenocarcinomas are not fully understood because they are rare. To clarify these characteristics, we performed genetic and epigenetic analysis of cancer-related genes in these lesions. One hundred and seven non-ampullary duodenal adenomas and intramucosal adenocarcinomas, including 100 small intestinal-type tumors (90 adenomas and 10 intramucosal adenocarcinomas) and 7 gastric-type tumors (2 pyloric gland adenomas and 5 intramucosal adenocarcinomas), were investigated. Using bisulfite pyrosequencing, we assessed the methylation status of CpG island methylator phenotype (CIMP) markers and MLH1. Then using next-generation sequencing, we performed targeted exome sequence analysis within 75 cancer-related genes in 102 lesions. There were significant differences in the clinicopathological and molecular variables between small intestinal-and gastric-type tumors, which suggests the presence of at least two separate carcinogenic pathways in non-ampullary duodenal adenocarcinomas. The prevalence of CIMP-positive lesions was higher in intramucosal adenocarcinomas than in adenomas. Thus, concurrent hypermethylation of multiple CpG islands is likely associated with development of non-ampullary duodenal intramucosal adenocarcinomas. Mutation analysis showed that APC was the most frequently mutated gene in these lesions (56/102; 55%), followed by KRAS (13/102; 13%), LRP1B (10/102; 10%), GNAS (8/102; 8%), ERBB3 (7/102; 7%), and RNF43 (6/102; 6%). Additionally, the high prevalence of diffuse or focal nuclear β-catenin accumulation (87/102; 85%) as well as mutations of WNT pathway components (60/102; 59%) indicates the importance of WNT signaling to the initiation of duodenal adenomas. The higher than previously reported frequency of APC gene mutations in small bowel adenocarcinomas as well as the difference in the APC mutation distributions between small intestinal-type adenomas and intramucosal adenocarcinomas may indicate that the adenoma-carcinoma sequence has only limited involvement in duodenal carcinogenesis.