ArticleMedical oncology (Northwood, London, England)2008
Molecular analysis of secondary kinase mutations in imatinib-resistant gastrointestinal stromal tumors.
Article in Medical oncology (Northwood, London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- The Evolving Role of Second- and Third-Generation Tyrosine Kinase Inhibitors in Gastrointestinal Malignancies: Advances in Targeted Therapy with Sunitinib, Regorafenib, and Avapritinib.Journal of clinical medicine · 2026Review
- Clinicopathological characteristics of progressive gastrointestinal stromal tumors and heterogeneity analyses of secondary mutations.The oncologist · 2025Article
- Advances in the research of the mechanism of secondary resistance to imatinib in gastrointestinal stromal tumors.Frontiers in oncology · 2022Review
- Sarcoma treatment in the era of molecular medicine.EMBO molecular medicine · 2020Review
- Prognostic Indicators for Gastrointestinal Stromal Tumors: A Review.Translational oncology · 2020Review
- A Novel System for Functional Determination of Variants of Uncertain Significance using Deep Convolutional Neural Networks.Scientific reports · 2020Article
- Loss of PI3 kinase association improves the sensitivity of secondary mutation of KIT to Imatinib.Cell & bioscience · 2020Article
- KRAS, KIT and TP53 mutations in mother's and daughter's gastric cardia adenocarcinomas.Przeglad gastroenterologiczny · 2018Article
- Tyrosine kinase inhibitor sensitive PDGFRΑ mutations in GIST: Two cases and review of the literature.Oncotarget · 2017Article
- Article
- Polyclonal SecondaryCancer discovery · 2017Article
- A meta-analysis of prognostic value of KIT mutation status in gastrointestinal stromal tumors.OncoTargets and therapy · 2016Article
- Detection of KIT and PDGFRA mutations in the plasma of patients with gastrointestinal stromal tumor.Targeted oncology · 2015Article
- Tumour heterogeneity and the evolution of polyclonal drug resistance.Molecular oncology · 2014Review
- Imatinib responsiveness in canine mast cell tumors carrying novel mutations of c-KIT exon 11.The Journal of veterinary medical science · 2014Article
- Targeted therapy for cancer: the gastrointestinal stromal tumor model.Surgical oncology clinics of North America · 2013Review
- Exploring novel therapeutic targets in GIST: focus on the PI3K/Akt/mTOR pathway.Current oncology reports · 2013Review
- Surgical intervention for imatinib and sunitinib-resistant gastrointestinal stromal tumors.International journal of clinical oncology · 2011Article
- Gastrointestinal stromal tumours: origin and molecular oncology.Nature reviews. Cancer · 2011Review
- Targeted therapy in GIST: in silico modeling for prediction of resistance.Nature reviews. Clinical oncology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most gastrointestinal stromal tumors (GISTs) are associated with activating kinase mutation in KIT or platelet-derived growth factor receptor alpha (PDGFRA) gene, and imatinib has revolutionized the care of advanced GISTs. However, most patients gradually developed resistance to imatinib. We intend to identify the secondary kinase mutations in imatinib-resistant GISTs and to study the relationship between secondary kinase mutations and the clinical response to imatinib. Twelve advanced GIST patients, who have developed resistance to imatinib were included in this study. Paraffin-embedded pretreatment GIST specimens and progression lesions of the tumors after resistance to imatinib were analyzed for kinase mutations in exons 9, 11, 13, and 17 of KIT gene and exons of 10, 12, 14, and 18 of PDGFRA gene. Primary KIT mutations have been found in all but one of the primary tumors including one case harboring de novo double KIT exon 11 mutations. Secondary kinase mutations in KIT and PDGFRA were found in seven and 1 of 12 patients, respectively. Two patients harbored more than one secondary KIT mutations in different progression sites, and there are four types of clonal or polyclonal evolution being observed. The secondary PDGFRA exon 14 mutation H687Y is a novel mutation that has never been reported before. Acquired secondary kinase mutations are the most important cause of secondary imatinib resistance in advanced GISTs. The identification of secondary kinase mutations is important in the development of new therapeutic strategies.
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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.