ArticleBMC cancer2009
Functional features of gene expression profiles differentiating gastrointestinal stromal tumours according to KIT mutations and expression.
Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Phase Ib Trial of the Combination of Imatinib and Binimetinib in Patients with Advanced Gastrointestinal Stromal Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- KITMolecular cancer therapeutics · 2021Article
- Clinicopathological value of long non-coding RNA profiles in gastrointestinal stromal tumor.PeerJ · 2021Article
- Article
- Identification of key genes and associated pathways in KIT/PDGFRA wild‑type gastrointestinal stromal tumors through bioinformatics analysis.Molecular medicine reports · 2018Article
- Tyrosine kinase inhibitor sensitive PDGFRΑ mutations in GIST: Two cases and review of the literature.Oncotarget · 2017Article
- Characterization and Targeting of Platelet-Derived Growth Factor Receptor alpha (PDGFRA) in Inflammatory Breast Cancer (IBC).Neoplasia (New York, N.Y.) · 2017Article
- Hedgehog pathway dysregulation contributes to the pathogenesis of human gastrointestinal stromal tumors via GLI-mediated activation of KIT expression.Oncotarget · 2016Article
- PDL1 expression is an independent prognostic factor in localized GIST.Oncoimmunology · 2015Article
- Post-transcriptional dysregulation by miRNAs is implicated in the pathogenesis of gastrointestinal stromal tumor [GIST].PloS one · 2013Article
- Bioinformatics and computational biology in Poland.PLoS computational biology · 2013Article
- Inactivation of Patched1 in mice leads to development of gastrointestinal stromal-like tumors that express Pdgfrα but not kit.Gastroenterology · 2013Article
- Genomic Grade Index predicts postoperative clinical outcome of GIST.British journal of cancer · 2012Article
- Genome-wide screening of genes regulated by DNA methylation in colon cancer development.PloS one · 2012Article
- Canine and human gastrointestinal stromal tumors display similar mutations in c-KIT exon 11.BMC cancer · 2010Article
- Gastrointestinal stromal tumours at present: an approach to burning questions.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2010Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastrointestinal stromal tumours (GISTs) represent a heterogeneous group of tumours of mesenchymal origin characterized by gain-of-function mutations in KIT or PDGFRA of the type III receptor tyrosine kinase family. Although mutations in either receptor are thought to drive an early oncogenic event through similar pathways, two previous studies reported the mutation-specific gene expression profiles. However, their further conclusions were rather discordant. To clarify the molecular characteristics of differentially expressed genes according to GIST receptor mutations, we combined microarray-based analysis with detailed functional annotations.
methodsTotal RNA was isolated from 29 frozen gastric GISTs and processed for hybridization on GENECHIP HG-U133 Plus 2.0 microarrays (Affymetrix). KIT and PDGFRA were analyzed by sequencing, while related mRNA levels were analyzed by quantitative RT-PCR.
resultsFifteen and eleven tumours possessed mutations in KIT and PDGFRA, respectively; no mutation was found in three tumours. Gene expression analysis identified no discriminative profiles associated with clinical or pathological parameters, even though expression of hundreds of genes differentiated tumour receptor mutation and expression status. Functional features of genes differentially expressed between the two groups of GISTs suggested alterations in angiogenesis and G-protein-related and calcium signalling.
conclusionOur study has identified novel molecular elements likely to be involved in receptor-dependent GIST development and allowed confirmation of previously published results. These elements may be potential therapeutic targets and novel markers of KIT mutation status.
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