The relationship of apocrine metaplasia to invasive breast cancer is contro
versial. Different authors have reported that apocrine differentiation in p
roliferative lesions may be a risk factor, a precursor lesion, or have no a
ssociation with malignancy. The aim of this study was to compare the geneti
c alterations in benign apocrine hyperplasia with apocrine ductal carcinoma
in situ (DCIS) and invasive apocrine carcinomas of the breast using compar
ative genomic hybridization, The mean number of alterations in apocrine hyp
erplasia 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 hy
perplasia 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 nu
mber changes. Apocrine hyperplasia is considered to be a benign lesion and
its relationship to invasive carcinoma remains unclear, Our data suggest th
at 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 apocrin
e carcinoma. These alterations are also commonly seen in nonapocrine breast
cancer. The data are consistent with apocrine hyperplasia as a putative no
nobligate precursor of apocrine carcinoma.