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Open AccessJournal ArticleDOI

Epithelial–mesenchymal plasticity in carcinoma metastasis

Jeff H. Tsai, +1 more
- 15 Oct 2013 - 
- Vol. 27, Iss: 20, pp 2192-2206
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TLDR
The functional requirement of EMT and/or MET during the individual steps of tumor metastasis is reviewed and the potential of targeting this program when treating metastatic diseases is discussed.
Abstract
Tumor metastasis is a multistep process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. Metastasis occurs through a series of steps: local invasion, intravasation, transport, extravasation, and colonization. A developmental program termed epithelial-mesenchymal transition (EMT) has been shown to play a critical role in promoting metastasis in epithelium-derived carcinoma. Recent experimental and clinical studies have improved our knowledge of this dynamic program and implicated EMT and its reverse program, mesenchymal-epithelial transition (MET), in the metastatic process. Here, we review the functional requirement of EMT and/or MET during the individual steps of tumor metastasis and discuss the potential of targeting this program when treating metastatic diseases.

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Dissertation

Role of Grb2 in myogenesis and epithelial-to-mesenchymal transition

Payal Mitra
TL;DR: This work presents a meta-analyses of Grb2 and its role in muscle differentiation and EMT, which shows clear relationships between the protein’s role in differentiation and the EMT mechanism.
Dissertation

Isolation, Detection and Functional Characterization of Circulating Tumor Cells Using Microfluidic-based Technologies

TL;DR: A two-dimensional separation approach that separates phenotypically-distinct subpopulations of cancer cells and identifies CTCs that have undergone the epithelial to mesenchymal transition (EMT), which can potentially be used for cancer prognostic profiling and therapeutic selection.
Journal ArticleDOI

Modeling the effects of EMT-immune dynamics on carcinoma disease progression.

TL;DR: In this paper, a multiscale evolutionary model was proposed to describe tumor-immune-EMT interactions and their impact on epithelial cancer progression from in situ to invasive disease.
Journal ArticleDOI

“Pulsed Hypoxia” Gradually Reprograms Breast Cancer Fibroblasts into Pro-Tumorigenic Cells via Mesenchymal–Epithelial Transition

TL;DR: In this paper , the authors investigate the intermediate phenotype of tumor cells undergoing the hypoxia-dependent transition from fibroblast to epithelial morphology, which can lead to pleotropic effects that potentially increase tumor aggressiveness and resistance to therapy through regulation of the expression of genes associated with the epithelial-mesenchymal transition (EMT) and mesenchymality transition (MET).
References
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Journal ArticleDOI

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TL;DR: Processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias and the identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes.
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