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Lookup NU author(s): Dr Dina Tiniakos
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The purpose of the study is to compare expression levels of I center dot R alpha, ER beta 1, ER beta 2 and cell proliferation marker Ki-67 in normal breast and hyperplastic and noninvasive neoplastic breast lesions.Routinely processed breast tissue from 55 patients provided 65 cases of noninvasive lesions, namely, epithelial hyperplasia of usual type (HUT), apocrine metaplasia (AM), atypical hyperplasia (AH) and ductal carcinoma in situ (DCIS) and 14 cases of adjacent normal breast tissue. Expression of ER alpha, ER beta 1 and ER beta 2 were evaluated using immunohistochemistry and correlated with Ki-67 labeling index (Ki-67 LI) and menopausal status of the patients.Compared with normal breast, ER alpha expression increased in low to intermediate-grade DCIS (DCIS1/2) and tended to decrease in high-grade DCIS, while ER beta 1 expression decreased in DCIS irrespective of grade. Mean Ki-67 LI in HUT, low to intermediate-grade DCIS and high-grade DCIS was higher than in normal breast. Higher than normal Ki-67 LI correlated with low ER beta 2 expression in the whole set of cases and with high ER alpha expression and low ER beta 2 expression in the postmenopausal cases of the subset that is generated by excluding AM and high-grade DCIS. Postmenopausal status correlated with low ER beta 1 expression in the whole set and with higher than normal Ki-67 LI, high ER alpha expression and low ER beta 1 expression in the subset.These findings are in accordance with an ER alpha-opposing oncosuppressive role of ER beta 2 in mammary carcinogenesis along the HUT-AH-DCIS1/2 pathway.
Author(s): Chantzi NI, Palaiologou M, Stylianidou A, Goutas N, Vassilaros S, Kourea HP, Dhimolea E, Mitsiou DJ, Tiniakos DG, Alexis IN
Publication type: Article
Publication status: Published
Journal: Journal of Cancer Research and Clinical Oncology
Year: 2014
Volume: 140
Issue: 6
Pages: 1057-1066
Print publication date: 01/06/2014
Online publication date: 27/03/2014
Acceptance date: 15/03/2014
ISSN (print): 0171-5216
ISSN (electronic): 1432-1335
Publisher: Springer
URL: http://dx.doi.org/10.1007/s00432-014-1652-0
DOI: 10.1007/s00432-014-1652-0
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