Abstract

Biomolecular evidence has shown that ductal carcinoma in situ(DCIS) may develop into invasive carcinoma of the canine mammary gland, and mutations in proto-oncogenes HER2 and EGFR; two members of the family of epidermal growth factor receptors, may be involved in this process. The purpose of this study was the characterization of the immunohistochemical expression of the EGFR and HER2 proteins in the process of neoplastic transformation, supposedly present in ductal carcinomas in situin canine mammary glands. Fifteen cases of DCIS were evaluated, with a higher expression of HER2 and EGFR being observed in low-grade carcinomas when compared with high-grade neoplasms, and with a high positive statistical correlation in the latter. Results suggest that aggressive tumors tend to lose the expression of EGFR and HER2 simultaneously. The loss of the expression of these markers may be related to the process of neoplastic progression in canine mammary tumors.

Highlights

  • Studies have shown that several non-neoplastic mammary intraepithelial lesions have been associated with the development of invasive mammary carcinomas

  • Biomolecular evidence has shown that ductal carcinoma in situ (DCIS) may develop into invasive carcinoma of the canine mammary gland, and mutations in proto-oncogenes HER2 and EGFR; two members of the family of epidermal growth factor receptors, may be involved in this process

  • The purpose of this study is to characterize the immunohistochemical expression of EGFR and HER2 in DCIS in canine mammary glands, with the aim to understand the role of DCIS in neoplastic progression

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Summary

Introduction

Studies have shown that several non-neoplastic mammary intraepithelial lesions have been associated with the development of invasive mammary carcinomas. Mutations in proto-oncogenes such as HER2 and EGFR, two members of the family of epidermal growth factor receptors, are among the main genetic changes related to the development of human cancer. The importance of these receptors has been extensively studied in human mammary neoplasms even originating treatment specific to inhibit its activity (Slamon et al, 1987; Tsutusui et al, 2002; Yaziji et al, 2004; Owens et al, 2004; Bhargava et al, 2005)

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