ArticleGenes, chromosomes & cancer2009
High density DNA array analysis reveals distinct genomic profiles in a subset of gastrointestinal stromal tumors.
Article in Genes, chromosomes & cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Gastrointestinal stromal tumors: diagnosis, therapy and follow-up care in Austria.Wiener medizinische Wochenschrift (1946) · 2013Guideline
- Linsitinib (OSI-906) for the Treatment of Adult and Pediatric Wild-Type Gastrointestinal Stromal Tumors, a SARC Phase II Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Trial
- ACRIN 6665/RTOG 0132 phase II trial of neoadjuvant imatinib mesylate for operable malignant gastrointestinal stromal tumor: monitoring with 18F-FDG PET and correlation with genotype and GLUT4 expression.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2012Trial
- Cytogenetic and molecular analyses of 291 gastrointestinal stromal tumors: site-specific cytogenetic evolution as evidence of pathogenetic heterogeneity.Oncotarget · 2022Article
- Somatic loss of function mutations in neurofibromin 1 and MYC associated factor X genes identified by exome-wide sequencing in a wild-type GIST case.BMC cancer · 2015Article
- Beyond standard therapy: drugs under investigation for the treatment of gastrointestinal stromal tumor.Expert opinion on investigational drugs · 2015Review
- Copy-neutral loss of heterozygosity and chromosome gains and losses are frequent in gastrointestinal stromal tumors.Molecular cancer · 2014Article
- Drug repurposing identifies a synergistic combination therapy with imatinib mesylate for gastrointestinal stromal tumor.Molecular cancer therapeutics · 2014Article
- Tumor-derived exosomes: A message delivery system for tumor progression.Communicative & integrative biology · 2014Review
- Novel pathways and molecular targets for the treatment of sarcoma.Current oncology reports · 2013Review
- Drug repurposing for gastrointestinal stromal tumor.Molecular cancer therapeutics · 2013Article
- Succinate dehydrogenase mutation underlies global epigenomic divergence in gastrointestinal stromal tumor.Cancer discovery · 2013Article
- Overexpression of insulin-like growth factor 1 receptor and frequent mutational inactivation of SDHA in wild-type SDHB-negative gastrointestinal stromal tumors.Genes, chromosomes & cancer · 2013Article
- Primary gastrointestinal stromal tumors: Current advances in diagnostic biomarkers, prognostic factors and management of its duodenal location.Intractable & rare diseases research · 2013Review
- Succinate dehydrogenase deficiency in pediatric and adult gastrointestinal stromal tumors.Frontiers in oncology · 2013Article
- Inactivation of Patched1 in mice leads to development of gastrointestinal stromal-like tumors that express Pdgfrα but not kit.Gastroenterology · 2013Article
- GSTT1 copy number gain and ZNF overexpression are predictors of poor response to imatinib in gastrointestinal stromal tumors.PloS one · 2013Article
- Bench to bedside and back again: personalizing treatment for patients with GIST.Molecular cancer therapeutics · 2011Article
- The emerging role of insulin-like growth factor 1 receptor (IGF1r) in gastrointestinal stromal tumors (GISTs).Journal of translational medicine · 2010Article
- Pediatric and wild-type gastrointestinal stromal tumor: new therapeutic approaches.Current opinion in oncology · 2010Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Gastrointestinal stromal tumors (GISTs) generally harbor activating mutations in KIT or platelet-derived growth facter receptor (PDGFRA). Mutations in these receptor tyrosine kinases lead to dysregulation of downstream signaling pathways that contribute to GIST pathogenesis. GISTs with KIT or PDGFRA mutations also undergo secondary cytogenetic alterations that may indicate the involvement of additional genes important in tumor progression. Approximately 10-15% of adult and 85% of pediatric GISTs do not have mutations in KIT or in PDGFRA. Most mutant adult GISTs display large-scale genomic alterations, but little is known about the mutation-negative tumors. Using genome-wide DNA arrays, we investigated genomic imbalances in a set of 31 GISTs, including 10 KIT/PDGFRA mutation-negative tumors from nine adults and one pediatric case and 21 mutant tumors. Although all 21 mutant GISTs exhibited multiple copy number aberrations, notably losses, eight of the 10 KIT/PDGFRA mutation-negative GISTs exhibited few or no genomic alterations. One KIT/PDGFRA mutation-negative tumor exhibiting numerous genomic changes was found to harbor an alternate activating mutation, in the serine-threonine kinase BRAF. The only other mutation-negative GIST with significant chromosomal imbalances was a recurrent metastatic tumor found to harbor a homozygous deletion in chromosome arm 9p. Similar findings in several KIT-mutant GISTs identified a minimal overlapping region of deletion of approximately 0.28 Mbp in 9p21.3 that includes only the CDKN2A/2B genes, which encode inhibitors of cell-cycle kinases. These results suggest that GISTs without activating kinase mutations, whether pediatric or adult, generally exhibit a much lower level of cytogenetic progression than that observed in mutant GISTs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.