ArticleBMC cancer2015
KIT exon 10 variant (c.1621 A > C) single nucleotide polymorphism as predictor of GIST patient outcome.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Broad spectrum of regorafenib activity on mutant KIT and absence of clonal selection in gastrointestinal stromal tumor (GIST): correlative analysis from the GRID trial.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Trial
- Genetic landscapes and curative effect of CAR T-cell immunotherapy in patients with relapsed or refractory DLBCL.Blood advances · 2023Article
- Targeted Next-Generation Sequencing of Thymic Epithelial Tumours Revealed Pathogenic Variants inCancers · 2022Article
- Prevalence and significance of M541L single nucleotide polymorphism in the central European cohort of gastrointestinal stromal tumor patients.Journal of cancer research and clinical oncology · 2021Article
- Stable expansion of high-grade serous ovarian cancer organoids requires a low-Wnt environment.The EMBO journal · 2020Article
- Adjuvant therapy with imatinib in gastrointestinal stromal tumors (GISTs)-review and perspectives.Translational gastroenterology and hepatology · 2019Review
- Using biology to guide the treatment of sarcomas and aggressive connective-tissue tumours.Nature reviews. Clinical oncology · 2018Review
- Gastrointestinal stromal tumors (GIST): Facing cell death between autophagy and apoptosis.Autophagy · 2017Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor genotype plays a crucial role in clinical management of GIST. Whether genetic polymorphism of KIT may influence GIST patient outcome is unclear.
methodsWe investigated the biological and clinical significance of the presence of KIT exon 10 variant (c.1621 A > C), KIT (L541), in a transfected cell line (3 T3 L541) and in two retrospectively collected series of 109 GIST patients in total. The control group consisted of 60 healthy donors collected at the French department of blood transfusion.
resultsIn the 3 T3 L541 cell line, KIT(L541) protein exhibited a spontaneous phosphorylation status comparable to that of wild-type KIT but displayed a phosphorylation pattern of AKT and ERK1/2 that was found similar to that of the classical mutated forms of the KIT receptor. Of 109 patients enrolled in this retrospective translational research study, 24 (22%) harboured KIT (L541), similarly to the control group of healthy donors (n = 10 of 60, 17%). A higher prevalence of the variant KIT (L541) was observed in patients with metastatic status at diagnosis (KIT (L541) correlated nine of 22 versus 15 of 87, p = 0.02). In addition, patients with KIT (L541) and localized GIST had a higher rate of relapse at 5 years and lower relapse free survival at 5 years in univariate, as well as in multivariate analysis. Response rate and duration of response to imatinib was similar in KIT (L541) and KIT (M541) patients.
conclusionKIT (L541) genotype is associated with a higher risk of metastasis at diagnosis and a higher risk of relapse in GIST patients.
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