Cell polarity, epithelial-mesenchymal transition, and cell-fate decision gene expression in ductal carcinoma in situ

Danila Coradini, Patrizia Boracchi, Federico Ambrogi, Elia Biganzoli, Saro Oriana

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Article number984346
JournalInternational Journal of Surgical Oncology
Volume2012
DOIs
Publication statusPublished - 2012

ASJC Scopus subject areas

  • Oncology
  • Surgery

Fingerprint Dive into the research topics of 'Cell polarity, epithelial-mesenchymal transition, and cell-fate decision gene expression in ductal carcinoma in situ'. Together they form a unique fingerprint.

Cite this