ArticleMolecular oncology2013
Are two better than one? A novel double-mutant KIT in GIST that responds to Imatinib.
Article in Molecular oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Recurrent gastrointestinal stromal tumor with c-KIT double exon mutations: A rare case report.CytoJournal · 2025Article
- Review
- Computational Alanine Scanning and Structural Analysis of the SARS-CoV-2 Spike Protein/Angiotensin-Converting Enzyme 2 Complex.ACS nano · 2020Article
- Mutational spectrum and classification of novel mutations in patients with metastatic gastrointestinal stromal tumours.International journal of oncology · 2020Article
- Molecular and functional characterization of a new 3' end KIT juxtamembrane deletion in a duodenal GIST treated with neoadjuvant Imatinib.Oncotarget · 2017Article
- Synchronous occurrence of gastrointestinal stromal tumor and acute myeloid leukemia: A case report and review of the literature.Oncology letters · 2016Article
- Smoothened (SMO) receptor mutations dictate resistance to vismodegib in basal cell carcinoma.Molecular oncology · 2015Article
- Are two better than one? A novel double-mutant KIT in GIST that responds to Imatinib.Molecular oncology · 2013Article
- Update on imatinib for gastrointestinal stromal tumors: duration of treatment.OncoTargets and therapy · 2013Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal stromal tumors carry in about 85% of the cases activating mutations in KIT gene. Generally only one KIT mutation is found in primary tumors and the majority of mutations affecting KIT exon 11 is sensitive to Imatinib. We report upon a GIST case harboring a double-mutant KIT gene at exon 11, which expresses a receptor bearing the known activating W557G mutation and a newly discovered missense Y578C alteration. The relative affinities for ATP and Imatinib of each single (W557G, Y578C) and double (W557G/Y578C) mutant KITs were predicted by in silico studies (computer-based molecular simulations), and compared with those obtained for known Imatinib sensitive and resistant KIT mutants. In parallel, biochemical analysis of the single and double KIT mutants expressed in mammalian cells was performed. Both the in-silico/in-vitro investigations showed constitutive activation and sensitivity to Imatinib of the yet mentioned Y578C mutation as well as of the double mutant, providing evidence that the concomitant presence of the W557G and Y578C mutations does not affect Imatinib response compare to the single mutations, in line with what observed in Imatinib treated patient.
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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.