| Literature DB >> 24674454 |
Stella Blandamura1, Lara Alessandrini2, Roberta Bertorelle3, Francesca Simonato1, Vincenza Guzzardo1, Elisa Valentini1, Imerio Angriman4, Ambrogio Fassina1.
Abstract
GISTs originating multifocally at different GI sites, in patients lacking familial syndromes, could be interpreted as recurrent/metastatic disease. MiR-221/222 have recently been identified as regulators of KIT expression in GISTs. We report the first case of synchronous GISTs in the stomach and duodenum concomitant with an ampullary adenocarcinoma. Different CD117 expression patterns could be related to different KIT mutational status in the two lesions: gastric GIST showed a dot-like pattern and lacked KIT mutations; duodenal GIST had a strong membranous expression pattern, likely due to KIT exon 9 duplication, which is associated with lower response to imatinib. MiR-221/222 were downregulated in GISTs as compared with normal tissue (p<0.05) and expressed increased levels in the gastric GIST as compared with duodenal one (p<0.05). Our data support an independent origin of the two GISTs. Determining whether these tumors are multiple primaries or recurrencies is helpful to predict their malignancy and to select proper treatment.Entities:
Keywords: Adenocarcinoma; GISTs; MiR-221/222; Mutation; Polyclonality
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Year: 2014 PMID: 24674454 DOI: 10.1016/j.prp.2014.01.019
Source DB: PubMed Journal: Pathol Res Pract ISSN: 0344-0338 Impact factor: 3.250