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.
Background Gastric adenocarcinoma of fundic-gland type (GA-FG) is a rare variant of gastric neoplasia. However, the etiology, classification, and clinicopathological features of gastric epithelial neoplasm of fundic-gland mucosa lineage (GEN-FGML; generic term of GA-FG related neoplasm) are not fully elucidated. We performed a large, multicenter, retrospective study to establish a new classification and clarify the clinicopathological features of GEN-FGML. Methods One hundred GEN-FGML lesions in 94 patients were collected from 35 institutions between 2008 and 2019. We designed a new histopathological classification of GEN-FGML using immunohistochemical analysis and analyzed via clinicopathological, immunohistochemical, and genetic evaluation. Results GEN-FGML was classified into 3 major types; oxyntic gland adenoma (OGA), GA-FG, and gastric adenocarcinoma of fundic-gland mucosa type (GA-FGM). In addition, GA-FGM was classified into 3 subtypes; Type 1 (organized with exposure type), Type 2 (disorganized with exposure type), and Type 3 (disorganized with non-exposure type). OGA and GA-FG demonstrated low-grade epithelial neoplasm, and GA-FGM should be categorized as an aggressive variant of GEN-FGML that demonstrated high-grade epithelial neoplasm (Type 2 > 1, 3). The frequent presence of GNAS mutation was a characteristic genetic feature of GEN-FGML (7/34, 20.6%; OGA 1/3, 33.3%; GA-FG 3/24, 12.5%; GA-FGM 3/7, 42.9%) in mutation analysis using next-generation sequencing. Conclusions We have established a new histopathological classification of GEN-FGML and propose a new lineage of gastric epithelial neoplasm that harbors recurrent GNAS mutation. This classification will be useful to estimate the malignant potential of GEN-FGML and establish an appropriate standard therapeutic approach.
Background Colorectal adenocarcinoma with enteroblastic differentiation (CAED) is a rare subtype of colorectal malignancy with expression of enteroblastic markers (glypican 3, SALL4, AFP); however, the clinicopathological and epidemiological features are not fully elucidated. Aims The aims of this study were to elucidate and establish the molecular and clinicopathological characteristics of CAED. Materials and Methods In addition to three cases recently diagnosed as CAED, colorectal carcinoma (CRC) with expression of enteroblastic markers were selected by using immunohistochemistry (IHC) on tissue microarrays of 988 advanced CRC. We employed next‐generation sequencing (NGS) and Sanger sequencing for the detection of genetic alterations. IHC for p53 and HER2, HER2‐FISH and MSI status was also investigated. Survival analyses for clinicopathological parameters were performed using Kaplan–Meier methods. Results Thirty‐nine cases (4.0%) were positive for at least one enteroblastic marker. Histological evaluation of the total of 42 cases revealed that 10 contained tumour cells with clear cytoplasm. Enteroblastic marker‐positive cases had aggressive behaviour and poor prognosis. NGS revealed TP53 as the most frequently mutated gene. The rate of HER2‐positive cases and MSI‐H cases was 9.5% (four of 42) and 12.2% (five of 41), respectively. Among these 42 cases, there were no molecular and clinicopathological differences according to the presence of tumour cells with clear cytoplasm. Conclusions Enteroblastic marker‐positive CRC could be grouped together as CAED regardless of clear cell cytoplasm. Using this definition, the frequency of CAED is 4.0% and has a poorer prognosis than that for conventional CRCs. HER2 targeted therapy would be a meaningful treatment for CAED, and CAEDs contain both MSI‐H and MSI‐stable CRCs, although the MSS phenotype is dominant.
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