Abstract
BackgroundKIT is a tyrosine kinase growth factor receptor. High expression of KIT has been found in several tumors including canine hemangiosarcoma (HSA). This study investigated the correlation of KIT expression and c-kit sequence mutations in canine HSAs and benign hemangiomas (HAs).ResultsImmunohistochemistry (IHC) staining confirmed KIT expression in 94.4 % (34/36) of HSAs that was significantly higher than 0 % in HAs (0/16). Sequencing the entire c-kit coding region of HSAs and normal canine cerebellums (NCCs) revealed GNSK-deletion in exon 9. As for exon 9 genotyping by TA-cloning strategy, GNSK-deletion c-kit accounted for 48.6 % (68/140) colonies amplified from12 KIT-positive HSAs, a significantly higher frequency than 14.1 % (9/64) of colonies amplified from six NCCs.ConclusionsDue to the distinct expression pattern revealed by IHC, KIT might be used to distinguish benign or malignant vascular endothelial tumors. Moreover, the high incidence of GNSK-deletion c-kit in canine HSAs implicates KIT isoforms as possibly participating in the tumorigenesis of canine HSAs.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-016-0772-y) contains supplementary material, which is available to authorized users.
Highlights
IntroductionHigh expression of KIT has been found in several tumors including canine hemangiosarcoma (HSA)
KIT is a tyrosine kinase growth factor receptor
KIT is activated by autophosphorylation upon the binding of its ligand stem cell factor (SCF) [5]; it is constitutively expressed in a number of cells including mast cells, and hematopoietic stem cells
Summary
High expression of KIT has been found in several tumors including canine hemangiosarcoma (HSA). This study investigated the correlation of KIT expression and c-kit sequence mutations in canine HSAs and benign hemangiomas (HAs). KIT protein, encoded by proto-oncogene c-kit, is a tyrosine kinase growth factor receptor for stem cell factor (SCF). KIT is activated by autophosphorylation upon the binding of its ligand SCF [5]; it is constitutively expressed in a number of cells including mast cells, and hematopoietic stem cells [6]. Sequence analysis of canine mast cell tumors (MCTs) identified several mutations in exons 8, 9, 11, and 17 of c-kit RNA [14]. In contrast to MCTs, no mutation was found in these two exons (11 and 17) of c-kit gene in KIT-positive neoplasms of vascular cell origin [7]
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