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1. Vet J. 2012 Mar 6. [Epub ahead of print]

Overexpression of P-glycoprotein, STAT3, phospho-STAT3 and KIT in spontaneous
canine cutaneous mast cell tumours before and after prednisolone treatment.

Teng SP, Hsu WL, Chiu CY, Wong ML, Chang SC.

Department of Veterinary Medicine, College of Veterinary Medicine, National Chung
Hsing University, Taichung 40227, Taiwan.

Prednisolone is a glucocorticoid (GC) commonly used in the treatment of canine
mast cell tumours (MCTs); however, resistance to GCs develops in many MCTs
following repeated treatment. P-glycoprotein (P-gp), signal transducer and
activator of transcription 3 (STAT3) and KIT (CD117) are involved in GC
resistance. The aim of this study was to evaluate the response to prednisolone
treatment in canine cutaneous MCTs and to investigate the levels of P-gp, STAT3,
phospho-STAT3 (pSTAT3) and KIT proteins in MCTs with or without prednisolone
treatment. Immunohistochemistry was performed on tumour samples from 41 dogs with
cutaneous MCTs. The overall objective response rate (including complete and
partial responses) was 51.8% for dogs treated with prednisolone; poorly
differentiated or higher stage MCTs had a lower response rate. The median
time-span of tumours to reach maximal tumour regression was 14d (range 3-77d); 22
(81.5%) reached maximal regression at 21d. The majority of MCTs overexpressed
both P-gp and STAT3 before and after prednisolone treatment. Reduced expression
of pSTAT3 and alterations in the KIT expression pattern were observed in MCTs
post-treatment. Prednisolone treatment that caused a marked reduction in tumour
volume was correlated with reduced pSTAT3 expression. A cytoplasmic KIT staining
pattern was correlated with a lower tumour response rate to prednisolone
treatment.

Crown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.

PMID: 22398132 [PubMed - as supplied by publisher]