Cadherin Switch in Tumor Progression
By R. Hazan, R. Qiao, Rinat Keren, I. Badano, K. Suyama. Annals of the New York Academy of Sciences, 2004
610 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f0680c358a5229b1f48d3f7958a399803260d43b
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In Molecular Biology
- Mahmut Yilmaz
- Julian Heuberger
- Alissa M. Weaver
- Gerhard Christofori
- W. Birchmeier
- F. van Roy
- G. Berx
- R. Weinberg
Citations in the corpus
- Involvement of members of the cadherin superfamily in cancer. (2009, background): “Cite this article as Cold Spring Harb Perspect Biol doi: 10.1101/cshperspect.a003129 N-cadherin and FGF2 synergistically increase migration, invasion, and secretion of extracellular proteases (Hazan et al. 2004).”
- Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling. (2010, background): “in carcinomas following a so-called cadherin switch (Wheelock and Johnson 2003; Hazan et al. 2004).”
- Matrix MetalloProteinases (MMPs) andTissue Inhibitors of MetalloProteinases (TIMPs): positive and negative regulators intumor cell adhesion (2010, neutral): “Loss of E-cadherin (epithelial cadherin) from the cell surface, commonly occursin epithelial tumors, leads to disruption of cell contacts, tumor cell detachment, shape change and local invasion, events that initiate a program named epithelial to mesenchymal transition (EMT)[6,8,9].”
- Expression profiling of ependymomas unravels localization and tumor grade‐specific tumorigenesis (2009, background): “This suggest weakening of intercellular junctions and cytoskeletal dissociation, facilitating tumor growth and progression.(46) FIGURE 4.”
- Tumor morphology and phenotypic evolution driven by selective pressure from the microenvironment. (2006, background): “For example, we introduced the possibility that tumor cell clones may express either of two distinct homotypic adhesion pairs (by analogy to the E- to N-cadherin switch that occurs in tumor progression; Hazan et al., 2004).”
- EMT, the cytoskeleton, and cancer cell invasion (2009, background): “Its expression is upregulated in the cells of the primitive streak during mesoderm formation and during progression of a variety of cancers, where its expression correlates with poor prognosis [74–76].”