Abstract
BackgroundFeline mammary carcinoma has been proposed as a natural model of highly aggressive, hormone-independent human breast cancer. To further explore the utility of the model by adding new similarities between the two diseases, we have analyzed the oncogene HER-2 status at both the protein and the gene levels.MethodsFormalin-fixed, paraffin-embedded tissue samples from 30 invasive carcinomas, 7 benign lesions and two normal mammary glands were analyzed. Tumour features with prognostic value were recorded. The expression of protein HER-2 was analyzed by immunohistochemistry and the number of gene copies by means of DNA chromogenic in situ hybridization.ResultsImmunohistochemical HER-2 protein overexpression was found in 40% of feline mammary carcinomas, a percentage higher to that observed in human breast carcinoma. As in women, feline tumours with HER-2 protein overexpression had pathological features of high malignancy. However, amplification of HER-2 was detected in 16% of carcinomas with protein overexpression, a percentage much lower than that observed in their human counterpart.ConclusionFeline mammary carcinoma would be a suitable natural model of that subset of human breast carcinomas with HER-2 protein overexpression without gene amplification.
Highlights
Feline mammary carcinoma has been proposed as a natural model of highly aggressive, hormone-independent human breast cancer
Human epidermal growth factor receptor type 2 (HER-2) protein overexpression is found in 15–30% of human breast carcinomas and comparative fluorescent in situ hybridization studies have shown that gene amplification is present in some 85–90% of the cases [2,3]
Protein HER-2 expression The HER-2 polyclonal antibody raised against the human antigen crossreacted with feline tissues as a low percentage of epithelial cells of non-altered ducts and acini from normal mammary glands showed a faint, barely perceptible staining in part of the cell membrane
Summary
Feline mammary carcinoma has been proposed as a natural model of highly aggressive, hormone-independent human breast cancer. To further explore the utility of the model by adding new similarities between the two diseases, we have analyzed the oncogene HER-2 status at both the protein and the gene levels. HER-2 protein overexpression is found in 15–30% of human breast carcinomas and comparative fluorescent in situ hybridization studies have shown that gene amplification is present in some 85–90% of the cases [2,3]. Chromogenic in situ hybridization (CISH) has been shown to have good correlation with FISH [4,5], which is currently regarded as a gold standard method for detecting HER-2 amplification, but it is not very practical for routine histopathological laboratories
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