ArticleGenes, chromosomes & cancer2013
Overexpression of insulin-like growth factor 1 receptor and frequent mutational inactivation of SDHA in wild-type SDHB-negative gastrointestinal stromal tumors.
Article in Genes, chromosomes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 70 citations in OpenAlex.
- Fibroblast growth factor receptor inhibition for succinate dehydrogenase-deficient gastrointestinal stromal tumors: a phase 2 trial.Nature medicine · 2026Trial
- 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
- Pathologic and molecular features correlate with long-term outcome after adjuvant therapy of resected primary GI stromal tumor: the ACOSOG Z9001 trial.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014Trial
- Establishment and genomic validation of novel patient-derived xenograft models for drug discovery in gastrointestinal stromal tumor.BMC cancer · 2026Article
- Advancement in medical treatment for gastrointestinal stromal tumors (GISTs): a ray of hope.Annals of medicine and surgery (2012) · 2025Review
- Gastrointestinal Malignancy: Genetic Implications to Clinical Applications.Cancer treatment and research · 2024Review
- Combined Inhibition of AKT and KIT Restores Expression of Programmed Cell Death 4 (PDCD4) in Gastrointestinal Stromal Tumor.Cancers · 2021Article
- Identification of Wee1 as a target in combination with avapritinib for gastrointestinal stromal tumor treatment.JCI insight · 2021Article
- Article
- Analysis of clinicopathologic features and gene mutations in gastrointestinal stromal tumor: a series of 58 patients.International journal of clinical and experimental pathology · 2021Article
- Interaction of germline variants in a family with a history of early-onset clear cell renal cell carcinoma.Molecular genetics & genomic medicine · 2019Article
- Identification of key genes and associated pathways in KIT/PDGFRA wild‑type gastrointestinal stromal tumors through bioinformatics analysis.Molecular medicine reports · 2018Article
- Targeting IGF1R pathway in cancer with microRNAs: How close are we?RNA biology · 2018Review
- The emerging role and targetability of the TCA cycle in cancer metabolism.Protein & cell · 2018Review
- Molecular characterization and pathogenesis of gastrointestinal stromal tumor.Translational gastroenterology and hepatology · 2018Review
- Succinate dehydrogenase deficiency in a PDGFRA mutated GIST.BMC cancer · 2017Review
- The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST).Journal of translational medicine · 2017Article
- SDHA related tumorigenesis: a new case series and literature review for variant interpretation and pathogenicity.Molecular genetics & genomic medicine · 2017Article
- Gastrointestinal stromal tumors (GIST): Facing cell death between autophagy and apoptosis.Autophagy · 2017Review
- Update on clinical research and state of the art management of patients with advanced sarcomas and GIST.ESMO open · 2016Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Approximately 15% of gastrointestinal stromal tumors (GISTs) in adults and 85% in children lack mutations in KIT and PDGFRA and are known as wild-type GISTs. Wild-type GISTs from adults and children express high levels of insulin-like growth factor 1 receptor (IGF1R) and exhibit stable genomes compared to mutant GISTs. Pediatric wild-type GISTs, GISTs from the multitumor Carney-Stratakis syndrome, and the Carney triad share other clinicopathological properties (e.g., early-onset, multifocal GISTs with epitheliod cell morphology), suggesting a common etiology. Carney-Stratakis is an inherited association of GIST and paragangliomas caused by germline mutations in succinate dehydrogenase (SDH) genes. The connection between defective cellular respiration and GIST pathology has been strengthened by the utilization of SDHB immunohistochemistry to identify SDH deficiency in pediatric GISTs, syndromic GISTs, and some adult wild-type GISTs. SDHB and IGF1R expression was examined in 12 wild-type and 12 mutant GIST cases. Wild-type GISTs were screened for coding-region alterations in SDH genes and for chromosomal aberrations using genome-wide single-nucleotide polymorphism and MIP arrays. SDHB-deficiency, identified in 11/12 wild-type GIST cases, was tightly associated with overexpression of IGF1R protein and transcript. Biallelic inactivation of the SDHA gene was a surprisingly frequent event, identified in 5 of 11 SDHB-negative cases, generally due to germline point mutations accompanied by somatic SDHA allelic losses. As a novel finding, inactivation of the SDHC gene from a combination of a heterozygous coding-region mutation and hypermethylation of the wild-type allele was found in one SDHB-negative case.
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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.