School of Veterinary Medical Science, University of Camerino, Matelica 62024, Italy.
Vet Res Commun. 2013 Jun;37(2):101-8. doi: 10.1007/s11259-013-9550-5. Epub 2013 Jan 13.
Several studies of canine spontaneous mast cell tumours have described mutations in the c-kit proto-oncogene. These mutations produce a constitutively activated product and have been suggested to play a role in the malignant transformation of mast cells. We hypothesize that the selective tyrosine kinase inhibitor imatinib mesylate inhibits signal transduction and induces apoptosis when tested in cutaneous canine mast cell tumour samples positive for mutation in c-kit exon 11. Three-dimensional ex vivo cultures of canine grade II mast cell tumour treated with STI-571 at 48, 72, and 96 h and tested for signal transduction and apoptosis using appropriate assays were used. There was a progressive and significant increase in caspase-3 and TUNEL-positive mast cells compared to the untreated cultures. Additionally, a concurrent reduced expression of Ki67 and BCL-2 was observed. Furthermore, the treated cultures showed a marked reduction of Kit expression. Our results demonstrate that STI-571 induces Caspase-dependent apoptosis in a canine neoplastic mast cells possessing mutations in c-kit exon 11.
几项关于犬自发性肥大细胞瘤的研究描述了 c-kit 原癌基因突变。这些突变产生了一种持续激活的产物,并被认为在肥大细胞的恶性转化中发挥作用。我们假设选择性酪氨酸激酶抑制剂伊马替尼甲磺酸盐可抑制信号转导,并在检测到 c-kit 外显子 11 突变的皮肤犬肥大细胞瘤样本中诱导细胞凋亡。使用适当的检测方法,对用 STI-571 处理的犬 2 级肥大细胞瘤的三维离体培养物进行了 48、72 和 96 小时的信号转导和细胞凋亡检测。与未处理的培养物相比,caspase-3 和 TUNEL 阳性肥大细胞的数量逐渐显著增加。此外,还观察到 Ki67 和 BCL-2 的表达同时减少。此外,处理后的培养物 Kit 表达明显减少。我们的结果表明,STI-571 可诱导携带 c-kit 外显子 11 突变的犬肿瘤肥大细胞发生 Caspase 依赖性凋亡。