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- Title
Activating GNAS and KRAS mutations in gastric foveolar metaplasia, gastric heterotopia, and adenocarcinoma of the duodenum.
- Authors
Matsubara, A; Ogawa, R; Suzuki, H; Oda, I; Taniguchi, H; Kanai, Y; Kushima, R; Sekine, S
- Abstract
Background:Heterotopic gastric-type epithelium, including gastric foveolar metaplasia (GFM) and gastric heterotopia (GH), is a common finding in duodenal biopsy specimens; however, there is still controversy regarding their histogenetic backgrounds.Methods:We analysed a total of 177 duodenal lesions, including 66 GFM lesions, 81 GH lesions, and 30 adenocarcinomas, for the presence of GNAS, KRAS, and BRAF mutations.Results:Activating GNAS mutations were identified in 27 GFM lesions (41%) and 23 GH lesions (28%). The KRAS mutations were found in 17 GFM lesions (26%) and 2 GH lesions (2%). A BRAF mutation was found in only one GFM lesion (2%). These mutations were absent in all 32 normal duodenal mucosa specimens that were examined, suggesting a somatic nature. Among the GFM lesions, GNAS mutations were more common in lesions without active inflammation. Analyses of adenocarcinomas identified GNAS and KRAS mutations in 5 (17%) and 11 lesions (37%), respectively. Immunohistochemically, all the GNAS-mutated adenocarcinomas diffusely expressed MUC5AC, indicating gastric epithelial differentiation.Conclusions:A significant proportion of GFM and GH harbours GNAS and/or KRAS mutations. The common presence of these mutations in duodenal adenoma and adenocarcinoma with a gastric epithelial phenotype implies that GFM and GH might be precursors of these tumours.
- Subjects
DUODENAL cancer; ADENOCARCINOMA; GENETIC mutation; METAPLASIA; TISSUE wounds; INFLAMMATION; IMMUNOHISTOCHEMISTRY; PHENOTYPES
- Publication
British Journal of Cancer, 2015, Vol 112, Issue 8, p1398
- ISSN
0007-0920
- Publication type
Article
- DOI
10.1038/bjc.2015.104