الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
The expression of PDGF and its receptors was investigated by immunohistochemical analysis by using 46 canine HSAs and 21 cutaneous HAs by utilizing anti-PDGF-BB, anti-PDGFRα, and anti-PDGFRβ antibodies as primary antibodies. Immunoreactivities were scored as strongly positive (>25% positive neoplastic cells), weakly positive (1-25% positive neoplastic cells), and negative. In cutaneous HA, 33.3% and 57.1% of cases were strongly and weakly positive, respectively, and 43.5% and 13.0% of HSAs were strongly and weakly positive for PDGF-BB, respectively. Moreover, 38.1% and 28.6% of cutaneous HAs cases were strongly and weakly positive, respectively, and 23.9% and 4.3% of HSAs cases were strongly and weakly positive, respectively, for PDGFRα. 35 HSAs cases (76.1%) were strongly positive, and the remaining 11 (23.9%) were weakly positive for PDGFRβ. In contrast, 18 (72.0%) cutaneous HAs were negative, and only 3cases (12.0%) were weakly positive, for PDGFRβ. The proportion of strongly positive cases of HSAs was significantly higher than that of cutaneous HA. Mutational analysis of PDGFRs was examined on 27 HSAs and 20 HA by direct DNA sequencing as one of the mechanisms driving receptors activation on PDGFR α exons 10, 12, 14, 17, 18, and 19 and PDGFR β exons 10, 12, 13, 14, 17 and 18. In HA, 1 missense mutation was detected in PDGFRα exon 18 and 1 in PDGFRβ exon 17. Two HSA cases had missense mutations in exon 14 and 1 in exon 17 of PDGFRβ. Thus, genomic mutation of PDGFRs was not the main mechanism driving the activation of receptors in HSA and HA.