| Literature DB >> 23820134 |
Masato Kobayashi1, Shiori Kuroki, Keita Ito, Akiko Yasuda, Harumi Sawada, Kenichiro Ono, Tsukimi Washizu, Makoto Bonkobara.
Abstract
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.Entities:
Keywords: Deletion mutation; Dog; Gastrointestinal stromal tumour; Imatinib; c-kit exon 11
Mesh:
Substances:
Year: 2013 PMID: 23820134 DOI: 10.1016/j.tvjl.2013.05.035
Source DB: PubMed Journal: Vet J ISSN: 1090-0233 Impact factor: 2.688