Epithelial-mesenchymal transitions in development and pathologies.

By J. P. Thiery. Current Opinion in Cell Biology, 2003

1,302 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/916fe99b3f27a1a771a558243c40ae477d4b848c

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Citations in the corpus

Dual regulation of Snail by GSK-3β-mediated phosphorylation in control of epithelial–mesenchymal transition (2004, background): “This mesenchymal–epithelial transition (MET), a reverse of EMT, occurs at various stages of morphogenesis and is also used by cancer cells that make up micrometastases to establish a secondary carcinom”
Migrating cancer stem cells — an integrated concept of malignant tumour progression (2005, background): “This phenomenon, referred to as the epithelial to mesenchymal transition (EMT), is considered to be a crucial event in malignanc”
Notch signalling in solid tumours: a little bit of everything but not all the time (2011, positive): “EMT is a prerequisite for the tumour cells to cross the basement membrane, enter into circulation and result in distant metastases (reviewed in Ref”
NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression (2004, neutral): “EMT also occurs during embryonic development and is regulated by an elaborate interplay of signaling pathways (12, 13, 15, 16).”
EMT and tumor metastasis (2015, background): “More recently, the role of adherent EMT in pathogenesis of fibrosis and metastasis of certain carcinogenic tumors has been described [1-13].”
Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis. (2006, neutral): “Many of these mechanisms involve growth factors that promote various signaling cascades through their cognate receptor tyrosine kinases (2, 20).”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, neutral): “First described in the 1980s as a cellular phenomenon in the primitive streak of chick embryos, EMT governs many developmental processes such as gastrulation, neural crest development, somite dissociation, and palate and lip fusion (1, 2).”
Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition. (2005, background): “This transition is characterized by the combined loss of epithelial cell junction proteins such as E-cadherin and the gain of mesenchymal markers such as vimentin or fibronectin (9).”
Complex networks orchestrate epithelial–mesenchymal transitions (2006, background): “The triggers and the signalling pathways that regulate EMT have been previously reviewe”
Non-Smad TGF-β signals (2005, background): “When E-cadherin levels drop inside the cell, the adherens junctions of polarized epithelial cells also dissolve, which is a second hallmark of EMT (Thiery, 2003).”
Distinct roles of Akt1 and Akt2 in regulating cell migration and epithelial–mesenchymal transition (2005, background): “In EMT, the expression of epithelial proteins (e.g., E-cadherin) is suppressed and the expression of mesenchymal genes (e.g., vimentin and N-cadherin) is enhanced (for reviews see Grunert et al., 2003; Thiery, 2003).”
TGFβ in Cancer (2008, background): “process during embryonic development and a pathological feature in neoplasia and fibrosis (Thiery, 2003).”
A natural antisense transcript regulates Zeb2/Sip1 gene expression during Snail1-induced epithelial-mesenchymal transition. (2008, background): “Epithelial–mesenchymal transition (EMT) is a cellular process characterized by the loss of epithelial features and the acquisition of a mesenchymal phenotype (Thiery 2003; Huber et al. 2005).”