Peer-reviewed veterinary case report
P-glycoprotein and STAT3 levels in dog skin mast cell tumors
By Teng, Shr-Ping et al.·Published in Veterinary journal (London, England : 1997)·2012·Department of Veterinary Medicine·View original on PubMed →
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Original publication title: Overexpression of P-glycoprotein, STAT3, phospho-STAT3 and KIT in spontaneous canine cutaneous mast cell tumours before and after prednisolone treatment.
- Species:
- dog
Plain-English summary
A group of dogs with skin tumors called mast cell tumors (MCTs) were treated with prednisolone, a common medication for these tumors. About 52% of the dogs showed some improvement, with most reaching their best response within three weeks. However, tumors that were more aggressive or poorly differentiated responded less well to the treatment. After treatment, changes in certain proteins related to drug resistance were observed, suggesting that some tumors may not respond effectively to prednisolone. Overall, while many dogs benefited from the treatment, the response varied based on the tumor's characteristics.
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Abstract
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.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/22398132/