This issue of The Breast includes an elegant study by Selim et al. 1 on c-myc gene amplification and protein overexpression in apocrine metaplasia (APM) and apocrine adenosis (AA) of the breast using paraffin-embedded tissue. 1 In their report, the authors observe that all cases of APM and AA harbored c-myc protein overexpression, but no definitive gene amplification was found. Most importantly, they observed that the percentage of cells expressing c-myc in APM and AA was significantly correlated with cell proliferation, as assessed by Ki-67 immunolabeling index. On the basis of their findings and of previously reported studies, the authors suggest that c-myc overexpression occurs in early stages of breast carcinogenesis, that c-myc gene amplification may be a late event, and that in APM and AA c-myc overexpression is related to cell proliferation 1 . Selim et al. 1 findings have brought to our attention two thorny but rather important issues regarding current concepts of apocrine changes and their association with breast carcinomas, and also the role of c-myc in breast carcinogenesis.
