The histologic spectrum of apocrine lesions of the breast

Abstract

New data on apocrine carcinoma of the breast, especially on its unusual pathogenesis, are the facts that justify this study. The aim of this study was to describe the morphological features in both benign apocrine lesions and invasive apocrine carcinomas of the breast. The following apocrine lesions were pointed out: cysts, metaplasia, adenosis, adenoma, borderline malignant lesion, intraductal carcinoma and invasive apocrine carcinoma. Surgical specimens of breast benign and malignant lesions were fixed in formalin, embedded in paraffin blocks and the slides were stained with HE, PAS and immuno- histochemical ABC complex methods, using primary antibodies against: p53, Ki-67, androgen receptor, and GCDFP-15. The criteria of apocrine lesions, as well as classification of apocrine carcinoma were pointed out also. In the discussion we cited literature data about incidence of apocrine lesions in the breast, immunohistochemical, ultrastructural and molecular characteristics of apocrine lesions focusing on differential diagnostic problems between apocrine and nonapocrine lesions, and benign versus malignant apocrine lesion. The authors have suggested that apocrine carcinoma represents unusual type of the breast carcinoma and which may origin from the following precancerous lesions: apocrine hyperplasia, apocrine adenosis, atypical apocrine adenosis and adenoma. Immunohistochemical markers for apocrine differentiation are: GCDFP-15 and androgen receptors. Ki-67 and p53 may be good markers for differentiation between benign and malignant breast apocrine lesions. Positively staining for androgen receptors, not only in apocrine carcinoma of the breast, but also in benign lesions, has led some authors to postulate a possible role of androgens in the stimulation of breast epithelium and the development of apocrine cells and apocrine carcinomas. However, in this stage the clinical significance remains uncertain and follow-up studies will be required to evaluate this issue.