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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Epithelial-to-mesenchymal transition in metaplastic breast carcinomas with chondroid differentiation: expression of

Katja Gwin1, Rebecca Buell-Gutbrod, Maria Tretiakova

  • 1Department of Pathology, University of Chicago, The University of Chicago Medical Center, 5841 South Maryland Avenue, Chicago, IL 60637-1470, USA. katja.gwin@uchospitals.edu

Applied Immunohistochemistry & Molecular Morphology : AIMM
|August 11, 2010
PubMed

Insights

Epithelial-to-mesenchymal transition (EMT) is active in metaplastic breast carcinomas with chondroid differentiation (MBCD). This process, involving Snail and E-cadherin, may drive tumor metastasis.

Area of Science:

  • Oncology
  • Cell Biology
  • Pathology

Background:

  • Epithelial-to-mesenchymal transition (EMT) is crucial for tumor progression.
  • Snail is a key regulator of EMT, down-regulating epithelial genes like E-cadherin.
  • Metaplastic breast carcinomas with chondroid differentiation (MBCD) exhibit features suggestive of EMT.

Purpose of the Study:

  • To investigate the role of EMT in MBCD.
  • To analyze the expression patterns of Snail and E-cadherin in MBCD.

Main Methods:

  • Immunohistochemistry was used to assess Snail and E-cadherin expression in 12 MBCD tumors.
  • Differential analysis focused on the interface between epithelial and metaplastic components.

Main Results:

  • Snail expression transitioned from cytoplasmic to nuclear from the epithelial to metaplastic component.
  • E-cadherin staining was present in the epithelial component and lost in the metaplastic component.
  • Loss of E-cadherin correlated inversely with active nuclear Snail expression.

Conclusions:

  • EMT is induced in MBCD.
  • EMT may contribute to the hematogenous metastasis frequently observed in MBCD.

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