Feline fibroadenomatous hyperplasia and mammary carcinoma

Abstract

Previous research has shown that feline mammary hyperplasia is related to progesterone-induced mammary growth hormone (GH) expression. The aim of the current study is to evaluate the expression of GH, growth hormone receptor (GHR), insulin like growth factor 1 (IGF-I) and the progesterone receptor (PR) in fibroadenomatous hyperplasia (FAH) and mammary carcinomas of cats using QPCR analysis. A downregulation of GHR (p= 0,008), IGF-I (p= 0,001) and PR (p= 0,000) was found in the group of animals with carcinomas compared to animals with FAH. The effects of progestin treatment or removal of the endogenous progesterone source by ovary(hyster)ectomy on the gene expression were also analysed. Animals with FAH who were treated with progestins showed an upregulation of GH (p= 0,028) in comparison to animals with FAH wich were not treated. Intact queens showed an upregulation of GHR (p= 0,013) and PR (p= 0,038). Finally the influence of the breed was analysed showing that Maine Coons had a higher expression of the reference gene β2 microglobulin (B2M) (p= 0,026), GH (p= 0,044) and GHR (p= 0,029) in compared to all breeds combined. Additional eight FAH tissues were immunohistological analysed for the progesterone receptor and compared to the QPCR data. All eight tissue samples were positive for PR, but they differed in location and intensity. The number of positive nuclei and their intensity was found to be the best way of comparing the IHC results with the QPCR data. Striking finding was that the positive nuclei were bigger and rounder in animals who had received progestins. This is interesting since progesterone and progestins normally have an autorepressing effect on the progesterone receptor expression. Further research is necessary to determine why this occurs. In conclusion can be said that hormones play an important role in the etiology of FAH considering the results found in this study.