title: Molecular cytogenetic comparison of apocrine hyperplasia and apocrine carcinoma of the breast.
abstract: 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.
authors.affiliation: Breast Molecular Pathology Group, Department of Histopathology, Royal Free and University College Medical School, University College London, London, United Kingdom.
authors.forename: C
authors.initials: C
authors.lastname: Jones
authors.forename: S
authors.initials: S
authors.lastname: Damiani
authors.forename: D
authors.initials: D
authors.lastname: Wells
authors.forename: R
authors.initials: R
authors.lastname: Chaggar
authors.forename: S R
authors.initials: SR
authors.lastname: Lakhani
authors.forename: V
authors.initials: V
authors.lastname: Eusebi
mesh_terms: D000328:Adult; D000368:Aged; D001050:Apocrine Glands / Q000737:chemistry / Q000378:metabolism / Q000473:pathology*; D001053:Apolipoproteins; D053399:Apolipoproteins D; D002352:Carrier Proteins / Q000032:analysis; D002869:Chromosome Aberrations; D020732:Cytogenetic Analysis; D003937:Diagnosis, Differential; D005260:Female; D006023:Glycoproteins; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D008297:Male; D026901:Membrane Transport Proteins; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000379:methods; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D011944:Receptors, Androgen / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D013544:Sweat Gland Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
chemical_list: C024328:APOD protein, human; D001053:Apolipoproteins; D053399:Apolipoproteins D; D002352:Carrier Proteins; D006023:Glycoproteins; D026901:Membrane Transport Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone