The interactome of BRCA1 exon 11-encoded region
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Dongyi Xu
PROVIDER: PXD078165 | iProX | Thu May 07 00:00:00 BST 2026
REPOSITORIES: iProX
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Project description:Background & Aims: In gastrointestinal stromal tumors (GIST) KIT exon 11 deletions are associated with poor prognosis. The aim of this study was to determine the gene expression profile of GIST carrying KIT exon 11 deletions and to identify genes associated with poor prognosis. Methods: Expression profiling was performed on 9 tumors with KIT exon 11 deletions and 7 without KIT exon 11 mutations using oligonucleotide microarrays. In addition, gene expression profiles for 35 GISTs were analysed by meta-analysis. Differentially expressed genes were identified and confirmed by qPCR. Expression of CD133 (prominin-1) protein (AC133) was also examined by tissue microarray (TMA) analysis of 204 GISTs from a population-based study in Western Sweden. Survival analysis was performed using Cox regression model. Results: Gene expression profiling, meta-analysis and qPCR demonstrated up-regulation of the stem cell marker CD133 in GIST carrying KIT exon 11 deletions. Immunohistochemical analysis on TMA confirmed CD133 expression in 28% of all tumors. CD133 positivity was frequent in gastric GIST (48%) versus small intestinal GIST (4%). CD133 positivity was also frequent in GIST with KIT exon 11 mutations (41%) compared to tumors with mutations in KIT exon 9, PDGFRA, or wild-type tumors (0-17%). There was no significant correlation between CD133 staining and NIH risk score. Survival analysis demonstrated significant correlation between presence of CD133 and shorter overall survival. Conclusions: The stem cell marker CD133 is expressed in a subset of predominantly gastric GIST with KIT exon 11 mutations and associated with poor prognosis.
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Project description:Background & Aims: In gastrointestinal stromal tumors (GIST) KIT exon 11 deletions are associated with poor prognosis. The aim of this study was to determine the gene expression profile of GIST carrying KIT exon 11 deletions and to identify genes associated with poor prognosis. Methods: Expression profiling was performed on 9 tumors with KIT exon 11 deletions and 7 without KIT exon 11 mutations using oligonucleotide microarrays. In addition, gene expression profiles for 35 GISTs were analysed by meta-analysis. Differentially expressed genes were identified and confirmed by qPCR. Expression of CD133 (prominin-1) protein (AC133) was also examined by tissue microarray (TMA) analysis of 204 GISTs from a population-based study in Western Sweden. Survival analysis was performed using Cox regression model. Results: Gene expression profiling, meta-analysis and qPCR demonstrated up-regulation of the stem cell marker CD133 in GIST carrying KIT exon 11 deletions. Immunohistochemical analysis on TMA confirmed CD133 expression in 28% of all tumors. CD133 positivity was frequent in gastric GIST (48%) versus small intestinal GIST (4%). CD133 positivity was also frequent in GIST with KIT exon 11 mutations (41%) compared to tumors with mutations in KIT exon 9, PDGFRA, or wild-type tumors (0-17%). There was no significant correlation between CD133 staining and NIH risk score. Survival analysis demonstrated significant correlation between presence of CD133 and shorter overall survival. Conclusions: The stem cell marker CD133 is expressed in a subset of predominantly gastric GIST with KIT exon 11 mutations and associated with poor prognosis. Tumors with and without KIT exon 11 deletion were compared using a common reference design.
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