ArticleThe Journal of veterinary medical science2014
Imatinib responsiveness in canine mast cell tumors carrying novel mutations of c-KIT exon 11.
Article in The Journal of veterinary medical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Mapping the Kinase Inhibitor Landscape in Canine Mammary Carcinoma: Current Status and Future Opportunities.Animals : an open access journal from MDPI · 2026Review
- Clinical Use of Molecular Biomarkers in Canine and Feline Oncology: Current and Future.Veterinary sciences · 2024Review
- Analysis of VEGFR-2 and PDGFR-β expression in canine splenic hemangiosarcoma to identify drug repositioning candidates.Brazilian journal of veterinary medicine · 2024Article
- Article
- Comparative aspects of mast cell neoplasia in animals and the role of KIT in prognosis and treatment.Veterinary medicine and science · 2020Review
- Deregulation of VEGFR-2 and PDGFR Expression and Microvascular Density in a Triple-Negative Model of Canine Malignant Mammary Tumors with Lymph Node or Lung Metastasis.Veterinary sciences · 2019Article
- Cutaneous mastocytosis with a mutation in the juxtamembrane domain of c-kit in a young laboratory beagle dog.Journal of toxicologic pathology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In 2 individual cases of canine mast cell tumors, we identified 2 novel c-KIT mutations in exon 11: a 9-base pair (bp) deletion (c.1663-1671del) and a point mutation (c.1676T>A). The 9-bp deletion mutation caused a loss of 3 amino acids, corresponding to p.Gln555_Lys557del, and the point mutation resulted in the substitution of valine by aspartic acid (p.Val559Asp) in the juxtamembrane domain of the protein. Imatinib mesylate, a therapeutic agent for canine mast cell tumors, was used to treat both tumors. Complete remission was achieved at 33 and 14 days after administration, respectively. However, in both cases, the therapeutic response subsequently tapered with the duration of remission lasting 66 and 255 days, respectively. Although these 2 novel c-KIT mutations in exon 11 were not confirmed to be gain-of-function mutations, a further study may help clarify relevance between mutations identified in this report and responsiveness.
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Registered trials
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