Duodenal gastric heterotopia, sporadic or fundic gland polyp-associated, frequently carries β-catenin mutation

Nakagawa, Miku; Kitazawa, Riko; Kondo, Takeshi; Ninomiya, Kosuke; Okita, Masayoshi; Haraguchi, Ryuma; Kitazawa, Sohei

doi:10.1007/s00428-014-1612-8

Cited by 8 publications

(10 citation statements)

References 11 publications

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“…Two foveolar-type adenomas showed CDX-2(-), MUC5AC(+), MUC6(-), and 2 pyloric gland adenomas showed CDX-2(-), MUC5AC(-), MUC6(+) (Figure 2B). GDM is frequently observed in gastric type adenoma and/or heterotopic gastric mucosa in the duodenum [35], and β-catenin expression is almost only in the membrane, but not the nucleus [36]. …”

Section: Resultsmentioning

confidence: 99%

The different pathogenesis of sporadic adenoma and adenocarcinoma in non-ampullary lesions of the proximal and distal duodenum

et al. 2017

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Non-ampullary duodenal adenoma with activation of Wnt/β-catenin signalling is common in familial adenomatous polyposis (FAP) patients, whereas sporadic non-ampullary adenoma is uncommon. The adenoma-carcinoma sequence similar to colon cancer is associated with duodenal tumors in FAP, but not always in sporadic tumors. We obtained 37 non-ampullary duodenal tumors, including 25 adenomas and 12 adenocarcinomas, were obtained from biopsies and endoscopic resections. We performed immunohistochemistry for β-catenin, the hallmark of Wnt activation, and aldehyde dehydrogenase 1 (ALDH1), a putative cancer stem cell marker. In non-ampullary lesions, abnormal nuclear localization of β-catenin was observed in 21 (84.0%) of 25 adenomas and 4 (33.3%) of 12 adenocarcinomas. In the proximal duodenum, nuclear β-catenin was less frequent in both adenomas and adenocarcinomas. Gastric duodenal metaplasia (GDM) was observed only in the proximal duodenum. All adenomas with GDM were the gastric foveolar and pyloric gland types, and showed only membranous β-catenin. The intestinal-type adenomas had nuclear β-catenin in the proximal and distal duodenum. ALDH1-positive cells were more frequent in adenocarcinomas than adenomas. Nuclear β-catenin accumulation frequently occurred in ALDH1-positive cells in adenoma, but not in adenocarcinoma. In the non-ampullary proximal duodenum, Wnt/β-catenin pathway activation was more closely associated with adenomas than adenocarcinomas, and while it might cooperate with ALDH1 in adenoma, it does not in adenocarcinoma. The pathogenesis thus may differ between sporadic adenoma and adenocarcinoma of non-ampullary duodenal lesions, especially in the proximal and distal duodenum.

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Section: Resultsmentioning

confidence: 99%

The different pathogenesis of sporadic adenoma and adenocarcinoma in non-ampullary lesions of the proximal and distal duodenum

et al. 2017

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“…Conversely, such molecular alterations are absent in peptic injury-related foveolar metaplasia. 68 Deeply located Brunner glands may also show various degrees of regenerative proliferation and reactive atypia and form Brunner gland hyperplasia/ hamartoma. 69 This diagnostic category is not well defined, and the use of 'Brunner gland proliferative lesions' as a generic term has been encouraged.…”

Section: Non-neoplastic Polypsmentioning

confidence: 99%

“…A further similarity with gastric FGPs is the detection of somatic CTNNB1 (β‐catenin) gene mutations, which implies the possibility of a neoplastic condition. Conversely, such molecular alterations are absent in peptic injury‐related foveolar metaplasia 68 . Deeply located Brunner glands may also show various degrees of regenerative proliferation and reactive atypia and form Brunner gland hyperplasia/hamartoma 69 .…”

Section: Non‐neoplastic Polypsmentioning

confidence: 99%

The pathology of gastric and duodenal polyps: current concepts

2020

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The liberal use of upper endoscopy has led to an increased detection of gastric and duodenal polyps, which are identified in as many as 6 and 4.6% of patient examinations, respectively. Gastroduodenal polyps are a heterogeneous group of lesions that can be neoplastic or non‐neoplastic (e.g. hyperplastic or heterotopical). Most polyps present characteristic topographical features, as well as endoscopic appearance and size. Evaluation of the surrounding mucosa is essential in assessing the underlying pathology (e.g. Helicobacter pylori, autoimmune gastritis or inherited polyposis syndromes). Phylogenetically, gastric and duodenal polyps can be classified according to the epithelial compartment from which they derive. Polyps that arise from the surface epithelium can either be of foveolar or intestinal type, and they can develop from either the native mucosa or the metaplastic epithelium (gastric intestinal metaplasia or duodenal foveolar metaplasia). Other polyps develop from the deeper glandular component, such as pyloric/oxyntic gland derived subtypes. In this review we focus upon epithelial polyps, with an emphasis on the most common and clinically relevant lesions, and present recently described entities.

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“…[12][13][14] Around 90% sporadic FGPs were found to have activating mutations of the beta-catenin (CTNNB1) gene. 12,[15][16][17] Given the clinical heterogeneity of FAP, it remains unclear if FGPs can predate colonic lesions in pediatric FAP patients, especially those with de novo mutations. Even though both sporadic and syndromic FGPs harbor activating mutations of Wnt pathway, morphologic manifestations resulted from mutations of different genes might exist.…”

Section: Introductionmentioning

confidence: 99%

“…12–14 Around 90% sporadic FGPs were found to have activating mutations of the beta-catenin ( CTNNB1 ) gene. 12,15–17…”

Section: Introductionmentioning

confidence: 99%

Fundic Gland Polyps in the Pediatric Population: Clinical and Histopathologic Studies

et al. 2017

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We retrospectively studied the clinical and histologic features of pediatric fundic gland polyps (FGPs) in 16 patients. FGPs had an endoscopic prevalence of 0.25% in 8527 pediatric gastric biopsies. Five patients had familial adenomatous polyposis (FAP). The median age of onset was 17.7 years in FAP and 17.3 years in sporadic patients. All syndromic patients were asymptomatic and FGPs were identified during surveillance for existing or concurrent colon polyps. They did not take antacids. In comparison, all 11 sporadic FGPs were identified during evaluation of symptomatic patients who had taken antacids (median duration 21 months). Syndromic FGPs can be multiple at single endoscopy and were more likely to recur, while sporadic FGPs were often single. None of the sporadic patients had recurrence of FGPs or a subsequent diagnosis of FAP during a median follow-up of 20.5 months. The dilated fundic glands were lined by parietal and chief cells only in a majority (22/41, 53.7%) of syndromic FGPs, while additional tall mucinous lining cells were found in all sporadic FGPs. Syndromic FGPs did not have parietal cell hypertrophy in the background oxyntic mucosa. Nuclear immunopositivity for beta-catenin was essentially absent in all the FGPs. In conclusion, FGPs were rare in pediatric patients. In syndromic patients, FGPs are asymptomatic and did not precede colon polyps. Prolonged antacid intake seems to be associated with development of sporadic FGPs. Cellular components of dilated fundic glands and background parietal cell hypertrophy can be useful features to eliminate concern for syndromic polyposis.

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Duodenal gastric heterotopia, sporadic or fundic gland polyp-associated, frequently carries β-catenin mutation

Cited by 8 publications

References 11 publications

The different pathogenesis of sporadic adenoma and adenocarcinoma in non-ampullary lesions of the proximal and distal duodenum

The different pathogenesis of sporadic adenoma and adenocarcinoma in non-ampullary lesions of the proximal and distal duodenum

The pathology of gastric and duodenal polyps: current concepts

Fundic Gland Polyps in the Pediatric Population: Clinical and Histopathologic Studies

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