Indian Journal of Pathology and Microbiology
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Year : 2012  |  Volume : 55  |  Issue : 4  |  Page : 443-449

Epithelial mesenchymal transition in urothelial carcinoma: Twist in the tale

Department of Histopathology, National Institute of Pathology, Safdarjang Hospital Campus, New Delhi, India

Correspondence Address:
Purnima Paliwal
Department of Histopathology, National Institute of Pathology, Safdarjang Hospital Campus, Post Box 4909, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.107777

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Context: Epithelial to mesenchymal transition (EMT) is a process involving conversion of cells from an epithelial to mesenchymal phenotype. The role of candidate genes promoting EMT and favoring a promigratory phenotype has been demonstrated in epithelial cancer. Existing scientific research has not yielded a clinically relevant biomarker with predictive capacity beyond grade and stage in bladder cancer. Aim: The purpose of this study is to evaluate the immunohistochemical expression pattern of a panel of epithelial and mesenchymal markers in paraffin-embedded archival material of primary urothelial carcinoma as evidence of EMT. Materials and Methods: Immunohistochemical expression of transcription factor twist, epithelial (E-cadherin, cytokeratin) and mesenchymal (vimentin, N-cadherin) markers was analyzed on archival paraffin-embedded tissue samples from 48 patients with diagnosis of primary urothelial carcinoma of bladder. Statistical Analysis: Karl Pearson's χ2 test was used to evaluate the association between the expression of immunohistochemical markers and various clinico-pathologic variables. Non-parametric Kendall's tau-b statistics was used to determine the correlation between categorical variables. Results and Conclusion: The study demonstrated statistically significant association of cytokeratin, E-cadherin, vimentin, and twist with stage and grade of bladder cancer. Since these markers form part of the spectrum of changes associated with EMT, the study establishes proof of concept of the existence of this process in vivo. A significant negative correlation was noted between the expression of twist and E-cadherin. Exploiting its role as a transcriptional repressor of E-cadherin, twist may prove to be a useful candidate for targeted therapy in urologic oncology.

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