Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli. Gastroenterology

University of Rochester, Rochester, New York, United States
Gastroenterology (Impact Factor: 16.72). 09/1997; 113(2):659-63. DOI: 10.1053/gast.1997.v113.pm9247488
Source: PubMed


Gastric adenocarcinoma has been previously recognized as a potential complication of familial adenomatous polyposis coli (APC) and attenuated forms of APC (AAPC). This tumor has only been reported to originate from adenomatous polyps of the gastric mucosa in these clinical conditions. There have been no previous case reports of gastric adenocarcinoma arising from the more commonly found fundic gland polyps associated with AAPC or APC. We report the first definitive case of gastric adenocarcinoma arising from a hyperplastic polyp of the fundis of a patient with AAPC.

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    • "The frequent finding of genetic alteration in familial adenomatous polyposis suggests that this polyp is neoplastic rather than hamartomatous origin.11 Recently, one series reported adenocarcinoma arising from FGPs in patients with familial adenomatous polyposis or attenuated familial adenomatous polyposis.12,13 FGPs especially in young age and multiple in number might be associated with familial adenomatous polyposis, and these cases were accompanied by dysplasia in up to 40%.14 "
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    ABSTRACT: Gastric protruding lesions are frequently encountered by health screening esophagogastroduodenoscopy. They can be classified into epithelial lesion and subepithelial lesion. Epithelial gastric lesions are generally divided into benign and malignant. Benign lesions include some types of polyps, i.e., hyperplastic polyp, fundic gland polyp, and gastric adenoma. Malignant lesions include carcinoid, early gastric cancer and advanced gastric cancer. They can be accurately diagnosed by magnifying endoscopy or narrow band imaging. Here, I will discuss benign and malignant epithelial lesions of the stomach.
    Clinical Endoscopy 05/2013; 46(3):243-7. DOI:10.5946/ce.2013.46.3.243
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    • "Similar to the duodenum, stomach is also a major site of morbidity and potential mortality in FAP.29 For unknown reasons, gastric cancer in FAP is increased in the some Asians (4.2% in Korea and 2.1% in Japan).28,29 And the site of gastric cancers occurring in AFAP and FAP patients were mostly from fundic gland polyps.29,30 Gastric cancer of adenomatous origin occurring sites other than fundus, especially in the antrum were rare.29 Despite routine endoscopic surveillance, gastric cancers tend to develop in fundic gland polyps in AFAP and FAP patients, and the malignant risk increased as the polyps got bigger.29 "
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    ABSTRACT: Attenuated familial adenomatous polyposis (AFAP) is a variant of familial adenomatous polyposis with fewer than one hundred colorectal polyps and a later age of onset of the cancer. Here, we report two cases of AFAP within family members. Each patient demonstrated the same novel germ line mutation in exon 15 of the adenomatous polyposis coli (APC) gene and was successfully managed with sulindac after refusal to perform colectomy: a 23-year-old man with incidentally diagnosed gastric adenoma and fundic gland polyps underwent colonoscopy, and fewer than 100 colorectal polyps were found; a 48-year-old woman who happened to be the mother of the 23-year-old man also showed fewer than 100 colorectal polyps on colonoscopy. Genetic analysis revealed a novel frameshift mutation in exon 15 of the APC gene. The deletion of adenine-guanine with the insertion of thymine in c.3833-3834 resulted in the formation of stop codon 1,287 in both patients. The patients were treated with sulindac due to their refusal to undergo colectomy. The annual follow-up upper endoscopy and colonoscopy in the following 2 years revealed significant regression of the colorectal polyps in both patients.
    Gut and liver 01/2013; 7(1):120-5. DOI:10.5009/gnl.2013.7.1.120 · 1.81 Impact Factor
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    • "Studies showed that mutations in TP53 are present in a range of 40%-70% of early and advanced gastric cancers, and inactivation of TP53 resulting from LOH is found in 60%-70% of intestinal-type gastric cancers, thus making this gene among the most frequently mutated genes in cancers (Hamilton & Meltzer, 2006; Werner et al., 2001). It was suggested that accumulation of mutations in TP53 is involved in initiating carcinogenic processes, though not all studies are in agreement with this hypothesis (Liu et al., 2001; Zwick et al., 1997). The expression of p53 protein can be easily detected by immunohistochemical staining, because mutations in TP53 gene increase the half-life of its product, and it was postulated that it could be used as a biomarker in a clinical setting (Zheng et al., 2004). "
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    Gastric Carcinoma - Molecular Aspects and Current Advances, 06/2011; , ISBN: 978-953-307-412-2
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