ArticlePathology oncology research : POR2020
Identifying Secondary Mutations in Chinese Patients with Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs) by Next Generation Sequencing (NGS).
Article in Pathology oncology research : POR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 23 citations in OpenAlex.
- KIT Mutation-NTRK fusion oncogenic driver switch: a novel mechanism of acquired imatinib resistance in GIST.NPJ precision oncology · 2026Article
- Germ cell immunoprofile and KIT exon 17 mutation guide rectification of seminoma misclassified as epithelioid gastrointestinal stromal tumor: A case report.Biomedical reports · 2026Article
- Clinicopathological characteristics of progressive gastrointestinal stromal tumors and heterogeneity analyses of secondary mutations.The oncologist · 2025Article
- Clinical Use of Liquid-Based Comprehensive Genomic Profiling in Gastrointestinal Stromal Tumors.Laboratory investigation; a journal of technical methods and pathology · 2025Article
- Entry of ZSWIM4 to the nucleus is crucial for its inhibition of KIT and BMAL1 in gastrointestinal stromal tumors.Cell & bioscience · 2024Article
- RAF1 facilitates KIT signaling and serves as a potential treatment target for gastrointestinal stromal tumor.Oncogene · 2024Article
- New Abdominal Mass After Surgery for Gastrointestinal Stromal Tumor: Desmoid-Type Fibromatosis Difficult to Distinguish from Mesenchymal Tumor - A Case Report.International medical case reports journal · 2024Article
- Computed tomography texture-based models for predicting KIT exon 11 mutation of gastrointestinal stromal tumors.Heliyon · 2023Article
- Precision Oncology in Gastrointestinal Stromal Tumors.Current oncology (Toronto, Ont.) · 2023Review
- Development of Highly Sensitive Digital Droplet PCR for Detection of cKIT Mutations in Circulating Free DNA That Mediate Resistance to TKI Treatment for Gastrointestinal Stromal Tumor (GIST).International journal of molecular sciences · 2023Article
- Article
- Rare clear cell odontogenic carcinoma associated with impacted tooth in a young patient: case report and literature review.Oral and maxillofacial surgery · 2022Review
- Article
- Advances in the research of the mechanism of secondary resistance to imatinib in gastrointestinal stromal tumors.Frontiers in oncology · 2022Review
- Low Distribution of TIM-3Journal of immunology research · 2021Article
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8 authors at 1 institution in 1 country.
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Abstract
The aim of this study was to characterize secondary kinase mutations in Chinese patients with imatinib-resistant gastrointestinal stromal tumors (GISTs). Mutations in receptor tyrosine kinase (KIT; exons 9, 11, 13, 14, 17, and 18) and platelet-derived growth factor-alpha (PDGFRA; exons 12, 14, and 18) were analyzed by direct sequencing. After imatinib treatment, 425 cancer-related target genes were analyzed by next generation sequencing (NGS) in imatinib-resistant patients. Correlation of sequencing results with clinicopathologic features were analyzed. We identified 320 patients with secondary acquired resistance. We determined that 65.63% (210/320) of resistant patients had secondary KIT mutations in exon 13 (n = 134), exon 14 (n = 10), or exon 17 (n = 66), and 4.38% (14/320) had additional PDGFRA mutations in exon 14 (n = 3) or exon 18 (n = 11). All secondary KIT mutations were missense mutations and were mostly located in kinase domains. Ninety-six imatinib-resistant GIST patients did not have secondary KIT or PDGFRA mutations. Common independent mutation events were found in retinoblastoma protein 1 (RB1) (18/96 cases), SWI/SNF-related matrix associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1) (16/96 cases), and myc-associated factor X (MAX) (10/96 cases). RB1 or SMARCB1 mutations coexisted with activation of other oncogenes in 6 or 15 cases, respectively. Multiple mutations were also seen in cases with MAX mutations. These mutations are frequently associated with clinicopathological factors. Secondary mutations of KIT/PDGFRA were the most important contributors in GISTs developing resistance to imatinib treatment. Additional genetic events including RB1, SMARCB1, and MAX except secondary KIT/PDGFRA mutations are the most common for GISTs to evolve into resistant disease. Clinical assessment of the effect of these mutations may benefit existing risk assessment models and selection of adjuvant therapies in GIST patients.
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