pubmed-article:12414520 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0032580 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0878500 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0920184 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0205422 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:12414520 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:12414520 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:12414520 | pubmed:dateCreated | 2002-11-4 | lld:pubmed |
pubmed-article:12414520 | pubmed:abstractText | Gastric fundic gland polyps (FGPs) occur in two distinct clinicopathological scenarios: sporadic and familial adenomatous polyposis (FAP) associated. FAP-associated FGPs arise through somatic second hit alterations of the adenomatous polyposis coli (APC) gene and frequently demonstrate epithelial dysplasia (Am J Pathol 2000, 157:747-754). Sporadic FGPs, in contrast, tend to contain beta-catenin gene mutations and only infrequently show dysplasia (Am J Pathol 2001, 158:1005-1010). However, sporadic FGPs with dysplasia have not been previously investigated. We studied 13 sporadic FGPs with surface/foveolar low-grade dysplasia or changes indefinite for dysplasia for alterations in the APC/beta-catenin pathway, using chromosome 5q allelic loss assays and direct DNA sequencing of the mutation cluster region in exon 15 of APC and the phosphorylation region in exon 3 of beta-catenin. In addition, to evaluate for possible additional genetic alterations in FGPs, all cases were evaluated for microsatellite instability using fluorescent-based amplification of a standard panel of five microsatellite markers. Alterations in APC were present in seven (53.8%) FGPs, including two cases with bi-allelic APC inactivation (truncating intragenic mutation plus 5q allelic loss), two cases with APC mutation only, and three cases with 5q allelic loss only. In contrast, only two (15.4%) FGPs contained stabilizing beta-catenin mutations. All 13 FGPs were microsatellite stable. These results indicate that sporadic FGPs with dysplasia/indefinite for dysplasia are molecularly similar to FAP-associated FGPs, and are dissimilar to the more common sporadic nondysplastic FGPs. Mutations in APC and beta-catenin, despite occurring in the same genetic pathway, show differing biological properties, a phenomenon that has previously been demonstrated in colorectal neoplasms. The lack of microsatellite instability in FGPs in this study and of K-ras mutations in a previous study suggests that secondary genetic alterations are rare in both dysplastic and nondysplastic FGPs. | lld:pubmed |
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pubmed-article:12414520 | pubmed:language | eng | lld:pubmed |
pubmed-article:12414520 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12414520 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:12414520 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12414520 | pubmed:month | Nov | lld:pubmed |
pubmed-article:12414520 | pubmed:issn | 0002-9440 | lld:pubmed |
pubmed-article:12414520 | pubmed:author | pubmed-author:HamiltonStanl... | lld:pubmed |
pubmed-article:12414520 | pubmed:author | pubmed-author:AbrahamSusan... | lld:pubmed |
pubmed-article:12414520 | pubmed:author | pubmed-author:WuTsung-TehTT | lld:pubmed |
pubmed-article:12414520 | pubmed:author | pubmed-author:ParkSeun JaSJ | lld:pubmed |
pubmed-article:12414520 | pubmed:author | pubmed-author:MugarteguiLil... | lld:pubmed |
pubmed-article:12414520 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12414520 | pubmed:volume | 161 | lld:pubmed |
pubmed-article:12414520 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12414520 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12414520 | pubmed:pagination | 1735-42 | lld:pubmed |
pubmed-article:12414520 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:12414520 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12414520 | pubmed:articleTitle | Sporadic fundic gland polyps with epithelial dysplasia : evidence for preferential targeting for mutations in the adenomatous polyposis coli gene. | lld:pubmed |
pubmed-article:12414520 | pubmed:affiliation | Department of Pathology, Division of Gastrointestinal/Liver Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. | lld:pubmed |
pubmed-article:12414520 | pubmed:publicationType | Journal Article | lld:pubmed |
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