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(American Journal of Pathology. 2001;158:207-214.)
© 2001 American Society for Investigative Pathology

Regular Articles

Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast

Chris Jones^*, Stefania Damiani, Dagan Wells, Ranbir Chaggar^§, Sunil R. Lakhani^* and Vincenzo Eusebi

From the Breast Molecular Pathology Group,^*
Department of Histopathology, Royal Free and University College Medical School, University College London, London, United Kingdom; the Section of Anatomical Pathology and Cytopathology "M. Malpighi",
Ospedale Bellaria, University of Bologna, Bologna, Italy; and the Human Genetics and Embryology Group,
Department of Obstetrics and Gynaecology, and The Ludwig Institute for Cancer Research,^§
University College London, London, United Kingdom

The relationship of apocrine metaplasia to invasive breast cancer is controversial. Different authors have reported that apocrine differentiation in proliferative lesions may be a risk factor, a precursor lesion, or have no association with malignancy. The aim of this study was to compare the genetic alterations in benign apocrine hyperplasia with apocrine ductal carcinoma in situ (DCIS) and invasive apocrine carcinomas of the breast using comparative genomic hybridization. The mean number of alterations in apocrine hyperplasia was 4.1 (n = 10) compared to 10.2 in apocrine DCIS (n = 10) and 14.8 (n = 4) in invasive carcinoma. The most common alterations in apocrine hyperplasia were gains of 2q, 13q, and 1p and losses of 1p, 17q, 22q, 2p, 10q, and 16q. Apocrine DCIS and invasive carcinomas showed gains of 1q, 2q, 1p, and losses of 1p, 22q, 17q, 12q, and 16q as their most common DNA copy number changes. Apocrine hyperplasia is considered to be a benign lesion and its relationship to invasive carcinoma remains unclear. Our data suggest that some apocrine hyperplasias may be clonal proliferations. The mean number of alterations are lower in apocrine hyperplasia, however the changes show considerable overlap with those identified in in situ and invasive apocrine carcinoma. These alterations are also commonly seen in nonapocrine breast cancer. The data are consistent with apocrine hyperplasia as a putative nonobligate precursor of apocrine carcinoma.

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