ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2017
Emergence of CTNNB1 mutation at acquired resistance to KIT inhibitor in metastatic melanoma.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2017. 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, 15 citations in OpenAlex.
- Melanoma genomics - will we go beyond BRAF in clinics?Journal of cancer research and clinical oncology · 2024Review
- Mutational Characterization of Cutaneous Melanoma Supports Divergent Pathways Model for Melanoma Development.Cancers · 2021Article
- Article
- Tumor genetic heterogeneity analysis of chronic sun-damaged melanoma.Pigment cell & melanoma research · 2020Article
- FGF2 Induces Resistance to Nilotinib through MAPK Pathway Activation in KIT Mutated Melanoma.Cancers · 2020Article
- Review
- Non-BRAF Mutant Melanoma: Molecular Features and Therapeutical Implications.Frontiers in molecular biosciences · 2020Review
- Acquisition of APOBEC Mutagenesis and Microsatellite Instability Signatures in the Development of Brain Metastases in Low-Grade, Early-Stage Endometrioid Endometrial Carcinoma.JCO precision oncology · 2020Article
- Identification and ranking of recurrent neo-epitopes in cancer.BMC medical genomics · 2019Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe KIT inhibitor, imatinib, has shown promising efficacy in patients with KIT-mutated melanoma; however, acquisition of resistance to imatinib occurs rapidly in the majority of patients. The mechanisms of acquired resistance to imatinib in melanoma remain unclear.
methodsWe analyzed biopsy samples from paired baseline and post-treatment tumor lesions in one patient with KIT-mutated melanoma who had had an initial objective tumor regression in response to imatinib treatment followed by disease progression 8 months later.
resultsTargeted deep sequencing from post-treatment biopsy samples detected an additional mutation in CTNNB1 (S33C) with original KIT L576P mutation. We examined the functional role of the additional CTNNB1 S33C mutation in resistance to imatinib indirectly using the Ba/F3 cell model. Ba/F3 cell lines transfected with both the L576P KIT mutation and the CTNNB1 S33C mutation demonstrated no growth inhibition despite imatinib treatment, whereas growth inhibition was observed in the Ba/F3 cell line transfected with the L576 KIT mutation alone.
conclusionsWe report the first identification of the emergence of a CTNNB1 mutation that can confer acquired resistance to imatinib. Further investigation into the causes of acquired resistance to imatinib will be essential to improve the prognosis for patients with KIT-mutated melanoma.
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