Journal
APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
Volume 18, Issue 6, Pages 526-531Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PAI.0b013e3181e8d54b
Keywords
breast; carcinoma; epithelial-to-mesenchymal transition; snail; metaplastic; matrix; chondroid differentiation
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Epithelial-to-mesenchymal transition (EMT) is a key process in tumor progression and is induced by the master regulator Snail, a transcription factor that down-regulates epithelial genes, including E-cadherin, and up-regulates mesenchymal genes. Metaplastic breast carcinomas with chondroid differentiation (MBCD) have an epithelial and a mesenchymal chondroid component, giving them morphologic features reminiscent of EMT. To determine whether EMT plays a role in MBCD, we differentially analyzed Snail and E-cadherin expression in 12 tumors by immunohistochemistry. The interface between the tumor components showed a transition from inactive cytoplasmic Snail expression in the carcinoma component to active nuclear Snail expression in the metaplastic cells. Membranous E-cadherin staining was present in the epithelial and absent in the metaplastic component, showing a gradual loss of expression at the interface. E-cadherin expression was inversely correlated with active nuclear Snail expression. Our results suggest that EMT is induced in MBCD and may contribute to their frequent hematogenous metastasis.
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