Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/33026
標題: Overexpression of P-glycoprotein, STAT3, phospho-STAT3 and KIT in spontaneous canine cutaneous mast cell tumours before and after prednisolone treatment
作者: Teng, Shr-Ping
Hsu, Wei-Li
Chiu, Cheng-Yang
Wong, Min-Liang
Chang, Shih-Chieh
關鍵字: Canine;Mast cell tumour;Drug-resistance;Glucocorticoid;Neoadjuvant chemotherapy;Tumour regression;STAT3
Project: Veterinary Journal, Volume 193, Issue 2, Page(s) 551–556.
摘要: 
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
14 d (range 3–77 d); 22 (81.5%) reached maximal regression at 21 d. 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.
URI: http://hdl.handle.net/11455/33026
ISSN: 1090-0233
DOI: 10.1016/j.tvjl.2012.01.033
Appears in Collections:獸醫學系所

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