Abstract
Epithelial Mesenchymal Transition (EMT) initially discovered as a key developmental mechanism is now shown to be indirectly involved in fibrosis and is contributing to the progression of carcinomas. Additionally, to transcription factors driving the morphological transition, novel mechanisms are now described to modulate the different features of the transition. The debate as to whether EMT is essential for the dissemination of carcinoma cells from the primary tumors is likely to be resolved soon, considering that EMT is not a linear transition from an epithelial to a mesenchymal state. Multiple intermediate states can be reached without involving the presence of some of known transcription factors initially described as indispensable for the acquisition of mesenchymal-like phenotypes.
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