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Citation
Tags
HERO ID
7353015
Reference Type
Journal Article
Title
Diminished number or complete loss of myoepithelial cells associated with metaplastic and neoplastic apocrine lesions of the breast
Author(s)
Tramm, T; Kim, JY; Tavassoli, FA
Year
2011
Is Peer Reviewed?
Yes
Journal
American Journal of Surgical Pathology
ISSN:
0147-5185
EISSN:
1532-0979
Volume
35
Issue
2
Page Numbers
202-211
Language
English
PMID
21263240
DOI
10.1097/PAS.0b013e31820598a2
Web of Science Id
WOS:000286581700004
Abstract
The presence of myoepithelial (ME) cells is considered an important feature in the vast majority of benign breast lesions. Recently, a case showing the absence of myoepithelium in a mammary duct with apocrine metaplasia was reported. To investigate the status of ME cells associated with apocrine metaplasia, the distribution of ME cells in 59 metaplastic and intraductal proliferative apocrine lesions was evaluated using immunohistochemical expression of p63 and Calponin. p63 showed a diminished number of ME cells and increased intermyoepithelial nuclear distance in ducts with all variants of apocrine metaplasia and proliferation compared with normal glands. In the majority of cases, Calponin showed a continuous ME layer. In 6 cases, including an apocrine papilloma, there were definitive ME gaps confirmed by both markers, in the absence of atypia and with preservation of the basement membrane. In all cases, there was frequent heterogeneity in the distribution of ME cells in ducts harboring apocrine cells and even in various papillae within papillary lesions. In summary, benign and noninvasive apocrine lesions can show reduction and occasional complete loss of ME cells. This observation is particularly important when evaluating apocrine papillary proliferations, in which the absence of ME cells may lead to overdiagnosis of atypia and/or malignancy. The observation suggests that at least 2 ME markers should be used when evaluating apocrine lesions, and that a malignant diagnosis should be based on features of the proliferating cells until more data become available on the significance, if any, of the absence of ME cells in apocrine lesions.
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