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- Open Access
Evaluation of c-KIT protein expression in canine mammary tumors
© Salvador et al; licensee BioMed Central Ltd. 2013
- Published: 4 April 2013
- Normal Breast
- Mammary Carcinoma
- Tyrosine Kinase Protein
- Mammary Epithelium
- Breast Epithelium
c-KIT is a proto-oncogene that synthesizes a tyrosine kinase protein responsible for cell growth. Higher expression of c-KIT protein in women normal breasts correlates with differentiation status of normal breast epithelium, while loss of c-KIT expression is observed during progression or malignant transformation of mammary epithelium. In bitches the role of this tyrosine kinase receptor has not been established. The aim of this study was to identify c-KIT protein expression in canine breast tissue and compared results with c-KIT expression status in human breast tissue.
c-KIT protein expression was assessed by immunohistochemistry in 26 canine mammary tumors samples and compared with normal mammary tissue, non-metastatic and metastatic mammary carcinomas. c-KIT expression was evaluated according to its pattern, as established in canine mast cell tumors (KIT I: perimembranous, KIT II: focal cytoplasmic and KIT III: diffuse cytoplasmic). Fisher exact test was used to determine the association between the categorical variables.
Metastatic carcinoma were correlated to pattern KIT II, non-metastatic carcinoma to pattern KIT I and normal breast to pattern KIT III (p<0,05).
Our results differ from c-KIT protein profiles and relation to prognosis reported in canine mast cell tumors, since normal canine breast tissue had a KIT III pattern, related to worst prognosis in mast cell tumors. However, c-Kit pattern is not described in human breast cancer and correlated to prognosis.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.