Analysis of genomic mutation and immunohistochemistry of platelet‐derived growth factor receptors in canine vascular tumours

• Published in: Veterinary & comparative oncology Vol. 13; no. 3; pp. 237 - 245
• Main Authors: Abou Asa, S., Mori, T., Maruo, K., Khater, A., El-sawak, A., Abd el-Aziz, E., Yanai, T., Sakai, H.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.09.2015
• Subjects: Animals; DNA Primers; dog; Dog Diseases - genetics; Dogs; Female; hemangioma; Hemangioma - genetics; Hemangioma - veterinary; hemangiosarcoma; Hemangiosarcoma - genetics; Hemangiosarcoma - veterinary; immunohistochemistry; Immunohistochemistry - veterinary; Japan; Male; Mutation; PDGFR; Polymerase Chain Reaction - veterinary; Protein-Tyrosine Kinases - genetics; Receptor, Platelet-Derived Growth Factor alpha - analysis; Receptor, Platelet-Derived Growth Factor alpha - genetics; Receptor, Platelet-Derived Growth Factor beta - analysis; Receptor, Platelet-Derived Growth Factor beta - genetics; Vascular Neoplasms - genetics; Vascular Neoplasms - veterinary; Japan; hemangioma; PDGFR; mutation; immunohistochemistry; dog; hemangiosarcoma
• ISSN: 1476-5810; 1476-5829
• DOI: 10.1111/vco.12035

We examined whether mutation of the platelet‐derived growth factor receptor protein tyrosine kinase (PDGFR)‐α and PDGFR‐β genes contributes to their overexpression in canine vascular tumours. Genomic sequences of trans‐ or juxtamembrane regions of PDGFR‐α and PDGFR‐β were analysed with immunohistochemical staining and polymerase chain reaction‐direct sequencing using DNA from paraffin‐embedded neoplastic tissues of 27 hemangiosarcomas (HSAs) and 20 hemangiomas (HAs). Immunohistochemically, 75% of the HA cases were positive for PDGFR‐α and almost most of the HA cases were negative for PDGFR‐β. Of the HSA cases, 55.6% were negative for PDGFR‐α and 63% were strongly positive for PDGFR‐β. Among the HA cases, 1 missense mutation was detected in PDGFR‐α exon 18 and 1 in PDGFR‐β exon 17. Two HSA cases had missense mutations in exon 14 and 1 in exon 17 of PDGFR‐β. Thus, genomic mutation of trans‐ or juxtamembrane regions of PDGFRs was not the main mechanism driving the activation of receptors in HSA and HA.