Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis.

By J. Christiansen, A. Rajasekaran. Cancer Research, 2006

1,066 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/647c3df15f6999ef8981030ad8f21064a99c1794

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

In Molecular Biology

In Oncology

Citations in the corpus

Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “…have both epithelial (cell–cell adhesion) and mesenchymal (migration) traits, hence allowing collective cell migration, as seen during migration of multicellular aggregates in the ECM (4) and clusters of CTCs in bloodstream of breast, lung, and prostate cancer patients (12–14) ( Figure 1A ).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “clustered heterogeneous epithelial cells [140].”
Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “Indeed, the relevance of EMT in human tumours is still a matter of considerable debate (Tarin et al., 2005; Thompson et al., 2005; Christiansen and Rajasekaran, 2006; Scheel et al., 2007; Talmadge, 2007), and some of these considerations await clarification and the development of appropriate in…”
Multi-step pericellular proteolysis controls the transition from individual to collective cancer cell invasion (2007, background): “S5 ) and of epithelial masses in ductal breast carcinoma in vivo”
Circulating tumor cells (CTC) detection: clinical impact and future directions. (2007, background): “As discussed previously, the most malignant CTC lose epithelial antigens (by EMT), which means that assays targeting epithelial cells in blood are susceptible to missing the detection of the most invasive tumor cells.”
E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “…dissemination from the primary tumour, it is also clear that tumour cell invasion can occur with fully intact and functional cell–cell adhesions, and that a partial transition or loosening of cell–cell contacts might be sufficient to facilitate invasion (Christiansen and Rajasekaran, 2006).”
Generation of Breast Cancer Stem Cells through Epithelial-Mesenchymal Transition (2008, background): “Although still controversial, this process is presumed to be required for tumor invasion and metastasis of carcinoma cells by promoting loss of contact inhibition, increased cell motility and enhanced invasiveness [33].”
Cancer invasion and the microenvironment: plasticity and reciprocity. (2011, positive): “This will identify EMT-dependent and -independent routes and niches of natural and therapy-induced plasticity of invasion and their contribution to metastatic dissemination (Christiansen and Rajasekaran, 2006).”
Epithelial-mesenchymal transition in breast cancer relates to the basal-like phenotype. (2008, positive): “Furthermore, although full EMT might not be easy to achieve in vivo (8, 27) it has been suggested that carcinosarcomas (also known as metaplasic carcinomas or spindle cell carcinomas) may represent true examples of complete EMT (12, 13).”
Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “…and/or Snail2 in EMT via signaling through their corresponding receptor tyrosine kinases, which in turn can activate phosphoinositide-3-kinase (PI3K) and Ras, which then activate mitogen-activated protein kinase (MAPK) leading directly to Snail1/2 upregulation (Christiansen and Rajasekaran, 2006).”
Collective cell migration in morphogenesis, regeneration and cancer (2009, background): “Indirect evidence for collective invasion of cancer cells is apparent from histopathological analysis of human cancer lesions, in which neoplastic multicellular strands and masses have crossed the tissue boundaries and have extended into the tumour stroma while retaining intact cell–cell junction”
Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype? (2007, background): “Despite the increasing evidence that EMT occurs in vivo , the influence of EMT in human tumours is currently a matter of controvers”