Source:http://linkedlifedata.com/resource/pubmed/id/20834236
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007586,
umls-concept:C0007634,
umls-concept:C0026882,
umls-concept:C0031437,
umls-concept:C0038351,
umls-concept:C0205087,
umls-concept:C0205430,
umls-concept:C0238198,
umls-concept:C0242793,
umls-concept:C0332281,
umls-concept:C0439799,
umls-concept:C0585064,
umls-concept:C1416655,
umls-concept:C1690540,
umls-concept:C1709474
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pubmed:issue |
2
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pubmed:dateCreated |
2011-2-3
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pubmed:abstractText |
In gastrointestinal stromal tumors (GISTs), the occurrence of an epithelioid/mixed phenotype has been correlated to PDGFRA mutations, gastric localization and favorable outcome. On the other hand, the prognostic significance of an epithelioid/mixed growth pattern occasionally observed in GISTs with KIT mutation is unclear. The aim of this study was to evaluate the prognostic significance of an epithelioid/mixed phenotype in correlation to anatomical localization, genotype, and expression of cell-cycle markers in a series of 116 primary GISTs with KIT mutation on a tissue microarray. Independent of their anatomical localization, the majority of KIT-mutated GISTs displayed a pure spindled phenotype (72%), with the remaining tumors showing an epithelioid/mixed growth pattern. In KIT-mutated GISTs from the stomach, the occurrence of an epithelioid/mixed growth pattern was significantly correlated with larger tumor diameters (P=0.005), higher mitotic counts (P=0.0001), high-risk category (P=0.001), higher expression of the G2-phase cell-cycle marker cyclin B1 (P=0.04), higher expression of the G1 to M-phase proliferation marker Ki67 (P=0.02) and a significantly shorter disease-free survival (P=0.003) compared with tumors with pure spindled morphology. In contrast, there were no significant differences between pure spindled and epithelioid/mixed GISTs from the small/large bowel. Our findings indicate that the epithelioid/mixed phenotype in KIT-mutant gastric GISTs represents a secondary tumor growth pattern associated with tumor progression and adverse outcome, probably through accelerated G1/S-phase restriction point passage.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1530-0285
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
248-55
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pubmed:meshHeading |
pubmed-meshheading:20834236-Cell Cycle,
pubmed-meshheading:20834236-Disease-Free Survival,
pubmed-meshheading:20834236-Epithelioid Cells,
pubmed-meshheading:20834236-Gastrointestinal Stromal Tumors,
pubmed-meshheading:20834236-Genotype,
pubmed-meshheading:20834236-Humans,
pubmed-meshheading:20834236-Immunohistochemistry,
pubmed-meshheading:20834236-Mutation,
pubmed-meshheading:20834236-Phenotype,
pubmed-meshheading:20834236-Prognosis,
pubmed-meshheading:20834236-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:20834236-Stomach Neoplasms,
pubmed-meshheading:20834236-Tissue Array Analysis,
pubmed-meshheading:20834236-Tumor Markers, Biological
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pubmed:year |
2011
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pubmed:articleTitle |
Epithelioid/mixed phenotype in gastrointestinal stromal tumors with KIT mutation from the stomach is associated with accelerated passage of late phases of the cell cycle and shorter disease-free survival.
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pubmed:affiliation |
Department of Pathology, Georg August University, Göttingen, Germany. florian.haller@uniklinik-freiburg.de
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pubmed:publicationType |
Journal Article
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