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Analysis of genomic mutation and immunohistochemistry of platelet‐derived growth factor receptors in canine vascular tumours
Author(s) -
Abou Asa S.,
Mori T.,
Maruo K.,
Khater A.,
Elsawak A.,
Abd elAziz E.,
Yanai T.,
Sakai H.
Publication year - 2015
Publication title -
veterinary and comparative oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 34
eISSN - 1476-5829
pISSN - 1476-5810
DOI - 10.1111/vco.12035
Subject(s) - missense mutation , exon , immunohistochemistry , growth factor receptor , biology , platelet derived growth factor receptor , mutation , cancer research , tyrosine kinase , microbiology and biotechnology , receptor , receptor tyrosine kinase , gene , pathology , growth factor , genetics , medicine , immunology
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 .