Epithelial-mesenchymal transitions: twist in development and metastasis.

By Yibin Kang, J. Massagué. Cell, 2004

1,615 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/7230454199beb04f299fafe183a582eb9dc28840

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Citations in the corpus

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): “The expression of Zeb-1 was recently shown to correlate with the degree of EMT in breast cancer cells (28), and E-cadherin has been shown to be highly regulated and repressed at the transcriptional level by factors including Snail, Slug, Twist, and ZEB (29, 30), likely requiring the recruitment of C”
NF-κB, an Active Player in Human Cancers (2014, positive): “Epithelial-mesenchymal transition (EMT) is an early event in metastasis (31).”
Epithelial–mesenchymal transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways (2005, background): “Cases of E-cadherin upregulation in tumor progression have been reported (Kang and Massague, 2004; Thiery and Morgan, 2004), specifically during intravasation and seeding of metastatic cells (see below).”
Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence. (2008, background): “Several groups have previously reported that high Twist1 expression promotes EMT and correlates with tumor invasion and metastasis in a variety of human cancers (Yang et al., 2004; Mironchik et al., 2005; Kang and Massague, 2004).”
Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis. (2006, background): “However, the mechanism by which Twist promotes EMT is poorly understood, as Twist is believed to function as a transcriptional activator when bound to E-box sequences (46).”
The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “…organs have already been established as a crucial character- istics of malignancy, whereas invasion and metastasis may predomi- nantly rely on the acquisition through the budding cancer cell bearing characteristics of EMT (Genetta, Ruezinsky, & Kadesch, 1994; Kang & Massagué, 2004; Thiery, 2002).”
Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “Also emphasizing the relationship between tumor dedifferentiation and EMT, the hedgehog and BMP-7 developmental signaling pathways are reactivated in aggressive prostate cancer and can induce EMT (Karhadkar et al., 2004; Yang et al., 2005).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “cancer appear to be related with common key players and regulators [8,9] suggesting that similarly to embryonic mesenchymal cells, EMT-”
Epithelial to Mesenchymal Transition Contributes to Drug Resistance in Pancreatic Cancer (2009, background): “The EMT phenotype is characterized by the loss of cell-to-cell adhesion with the disintegration of tight, adherens, and gap junctions and a phenotypic change from an ‘‘epithelial’’ morphology to a motile, fibroblast-like morphology (10, 11).”
The mesenchymal cell, its role in the embryo, and the remarkable signaling mechanisms that create it (2005, methodology): “For further discussion of EMT pathology, the reader is referred to reviews by Kinzler and Vogelstein (1997), Tan et al. (2001), Thiery (2002), Yang et al. (2004), and Kang and Massague (2004).”