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International Journal of Surgical Oncology
Volume 2012, Article ID 984346, 9 pages
Research Article

Cell Polarity, Epithelial-Mesenchymal Transition, and Cell-Fate Decision Gene Expression in Ductal Carcinoma In Situ

1Department of Work Medicine “Clinica del Lavoro L. Devoto”, Section of Medical Statistics and Biometry “G.A. Maccacaro”, University of Milano, 20133 Milan, Italy
2Senology Center, Casa di Cura Ambrosiana, Istituto Sacra Famiglia, Cesano Boscone, 20090 Milano, Italy

Received 29 November 2011; Revised 17 January 2012; Accepted 25 January 2012

Academic Editor: Lucio Fortunato

Copyright © 2012 Danila Coradini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Loss of epithelial cell identity and acquisition of mesenchymal features are early events in the neoplastic transformation of mammary cells. We investigated the pattern of expression of a selected panel of genes associated with cell polarity and apical junction complex or involved in TGF-β-mediated epithelial-mesenchymal transition and cell-fate decision in a series of DCIS and corresponding patient-matched normal tissue. Additionally, we compared DCIS gene profile with that of atypical ductal hyperplasia (ADH) from the same patient. Statistical analysis identified a “core” of genes differentially expressed in both precursors with respect to the corresponding normal tissue mainly associated with a terminally differentiated luminal estrogen-dependent phenotype, in agreement with the model according to which ER-positive invasive breast cancer derives from ER-positive progenitor cells, and with an autocrine production of estrogens through androgens conversion. Although preliminary, present findings provide transcriptomic confirmation that, at least for the panel of genes considered in present study, ADH and DCIS are part of a tumorigenic multistep process and strongly arise the necessity for the regulation, maybe using aromatase inhibitors, of the intratumoral and/or circulating concentration of biologically active androgens in DCIS patients to timely hamper abnormal estrogens production and block estrogen-induced cell proliferation.