Cell cycle alterations and their relationship to proliferation in apocrine adenosis of the breast

Article


Elayat, G., Selim, A. and Wells, C. 2009. Cell cycle alterations and their relationship to proliferation in apocrine adenosis of the breast. Histopathology. 54 (3), pp. 348-354. https://doi.org/10.1111/j.1365-2559.2009.03223.x
TypeArticle
TitleCell cycle alterations and their relationship to proliferation in apocrine adenosis of the breast
AuthorsElayat, G., Selim, A. and Wells, C.
Abstract

Aims: Apocrine adenosis (AA) is generally considered a benign disease of the breast. However, recent studies have suggested a precancerous potential for some of these lesions. The aim was to investigate the status of cell cycle proteins previously reported to be deregulated in breast cancer to identify their possible role in AA.

Methods and results: The cases were categorized into AA without atypia (NAA) and atypical AA (AAA). Using immunohistochemistry, the expression of cyclin D1, cyclin A, p27, p21, p16, pRb and Ki67 was determined in 29 NAA and 16 AAA cases. Cyclin D1, p21 and cyclin A were overexpressed in 58.6%, 51.7% and 31.8% of the NAA cases, respectively, whereas 81.3%, 62.5% and 41.7% of the AAA cases showed overexpression of cyclin D1, p21 and cyclin A, respectively. All cases were negative for p16, whereas pRb was expressed in all cases. Furthermore, proliferation in AA (4.5%) was significantly higher than that of normal breast epithelium (1%). There was no statistical significance in the degree of proliferation between the NAA (3.7%) and AAA (4.8%) groups.

Conclusions: The study indicates that NAA and AAA are biologically similar. A subset of AA defined by increased proliferation and significant cell cycle alterations may be susceptible to oncogenesis.

LanguageEnglish
PublisherWiley
JournalHistopathology
ISSN0309-0167
Electronic1365-2559
Publication dates
Print10 Feb 2009
Publication process dates
Accepted15 Aug 2008
Deposited26 Sep 2023
Output statusPublished
Digital Object Identifier (DOI)https://doi.org/10.1111/j.1365-2559.2009.03223.x
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