Imatinib-associated tumour response in a dog with a non-resectable gastrointestinal stromal tumour harbouring a c-kit exon 11 deletion mutation

A 10-year-old female Miniature Dachshund with a non-resectable gastrointestinal stromal tumour was treated with imatinib. The neoplastic cells had a deletion mutation (c.1667_1672del) within exon 11 of the c-kit gene, which resulted in deletion of three amino acids and insertion of one amino acid (p...

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Bibliographic Details
Published in:The veterinary journal (1997) 2013-10, Vol.198 (1), p.271-274
Main Authors: Kobayashi, Masato, Kuroki, Shiori, Ito, Keita, Yasuda, Akiko, Sawada, Harumi, Ono, Kenichiro, Washizu, Tsukimi, Bonkobara, Makoto
Format: Article
Language:English
Subjects:
amino acids
Animals
Antineoplastic Agents - therapeutic use
Base Sequence
Benzamides - therapeutic use
c-kit exon 11
carcinogenesis
Dachshund
Deletion mutation
Dog
Dog Diseases - drug therapy
Dog Diseases - genetics
Dog Diseases - pathology
Dogs
Exons
Female
Gastrointestinal Stromal Tumors - drug therapy
Gastrointestinal Stromal Tumors - genetics
Gastrointestinal Stromal Tumors - pathology
Gastrointestinal Stromal Tumors - veterinary
Gastrointestinal stromal tumour
gastrointestinal system
genes
Imatinib
Imatinib Mesylate
neoplasms
Piperazines - therapeutic use
Polymerase Chain Reaction - veterinary
Protein Kinase Inhibitors - therapeutic use
Proto-Oncogene Proteins c-kit - genetics
Proto-Oncogene Proteins c-kit - metabolism
Pyrimidines - therapeutic use
remission
Sequence Deletion
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Summary:A 10-year-old female Miniature Dachshund with a non-resectable gastrointestinal stromal tumour was treated with imatinib. The neoplastic cells had a deletion mutation (c.1667_1672del) within exon 11 of the c-kit gene, which resulted in deletion of three amino acids and insertion of one amino acid (p.Trp556_Val558delinsPhe) in the juxtamembrane domain of KIT. Following treatment with imatinib, the dog achieved partial remission on Day 21 with a continuous decrease in tumour size until Day 67 of treatment. Although no additional decrease in size was observed after Day 67 of treatment, the tumour remained stable in size as of Day 140 of treatment. The c-kit mutation found in the tumour cells appears to be a mutation driving oncogenesis, as evidenced by the partial remission elicited by imatinib in this dog.
ISSN:1090-0233
1532-2971
DOI:10.1016/j.tvjl.2013.05.035