ArticleOncoTargets and therapy2015
Inactivity of imatinib in gastrointestinal stromal tumors (GISTs) harboring a KIT activation-loop domain mutation (exon 17 mutation pN822K).
Article in OncoTargets and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- RNA-Based and DNA-Based Next-Generation Sequencing of KIT and PDGFRA Mutations in Gastrointestinal Stromal Tumors: Analytical Performance and Epidemiologic Insights.Translational oncology · 2026Article
- Therapeutic Management of Metastatic Thymoma and Thymic Carcinoma.Current oncology reports · 2025Review
- Concurrent Coprimary KIT Exon 17 and BRAF Mutations in a Small Intestinal GI Stromal Tumor-A Case Report.Journal of gastrointestinal cancer · 2025Article
- Gastrointestinal stromal tumors with an uncommon primary mutation responded well to imatinib.Cancer pathogenesis and therapy · 2025Article
- Article
- New C3H KitScientific reports · 2022Article
- Article
- Preoperative adjuvant therapy for locally advanced and recurrent/metastatic gastrointestinal stromal tumors: a retrospective study.World journal of surgical oncology · 2020Article
- Predictive biomarkers and tumor microenvironment in female genital melanomas: a multi-institutional study of 55 cases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Recent Progress of Targeted G-Quadruplex-Preferred Ligands Toward Cancer Therapy.Molecules (Basel, Switzerland) · 2019Review
- A meta-analysis of prognostic value of KIT mutation status in gastrointestinal stromal tumors.OncoTargets and therapy · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of gastrointestinal stromal tumors (GISTs) is largely driven by mutations in the KIT and PDGFRα genes. Imatinib mesylate is an oral small molecular tyrosine kinase inhibitor that mainly targets abl, c-KIT, and PDGFRα. Imatinib achieves disease control in approximately 70%-85% of patients with advanced GIST, and the median progression-free survival is 20-24 months. The efficacy of imatinib correlates with tumor kinase mutational status (exon 11 mutations mainly), and some mutations are known to be responsible for primary and secondary imatinib resistance. Beyond these, there are many other mutations that are considered rare and are associated with unknown clinical behavior. In the literature, there are poor and inconsistent data about the inhibitor sensitivity of mutations occurring in the activation-loop domain encoded by exon 17. In this article, we focus on a case of a patient suffering from GIST, harboring an extremely rare KIT activation-loop domain mutation (exon 17 mutation pN822K) treated with imatinib. A review of the literature is also presented.
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