Department of Veterinary Clinical Pathology, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo 180-8602, Japan.
Vet J. 2013 Oct;198(1):271-4. doi: 10.1016/j.tvjl.2013.05.035. Epub 2013 Jun 29.
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.
一只十岁雌性迷你腊肠犬患有不可切除的胃肠道间质肿瘤，接受了伊马替尼治疗。肿瘤细胞在 c-kit 基因的外显子 11 中发生缺失突变（c.1667_1672del），导致三个氨基酸缺失和一个氨基酸插入（p.Trp556_Val558delinsPhe），位于 KIT 的跨膜结构域。在接受伊马替尼治疗后，该犬在第 21 天达到部分缓解，肿瘤大小持续减小，直至治疗第 67 天。尽管在治疗第 67 天后未观察到肿瘤大小进一步减小，但肿瘤大小在治疗第 140 天仍保持稳定。在肿瘤细胞中发现的 c-kit 突变似乎是一种驱动肿瘤发生的突变，因为该犬对伊马替尼的部分缓解证实了这一点。
