Epithelial–mesenchymal transitions in tumour progression

By J. P. Thiery. Nature Reviews. Cancer, 2002

6,912 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2f3331eb7cbb1acc02b636cadc99d17565b02c86

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

1. M. Nieto
2. R. Weinberg
3. Peter Friedl
4. Raghu Kalluri
5. E. Hay
6. Jing Yang
7. M. Cristina Marchetti
8. J. Massagué

In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Jing Yang
4. Thomas Brabletz
5. J. Massagué
6. Raghu Kalluri
7. J. P. Thiery
8. K. Yeung

In Oncology

1. R. Weinberg
2. M. Nieto
3. J. Massagué
4. Jing Yang
5. Thomas Brabletz
6. E. Hay
7. J. P. Thiery
8. Raghu Kalluri

Citations in the corpus

• Role of tissue stroma in cancer cell invasion (2003, background): “During gastrulation epithelial cells in the ectoderm change into mesenchymal cells, which invade through the primitive streak and insert themselves between the ectoderm and the endoderm [19].”
• Cadherins in development: cell adhesion, sorting, and tissue morphogenesis. (2006, neutral): “Decreased E-cadherin gene transcription results in a loss of cell–cell adhesion and increased cell migration (Thiery 2002), as well as accumulation of cytoplasmic, signalingcompetent -catenin that may function independently of, or synergize with Wnt signaling (Ciruna and Rossant 2001).”
• Tumor cell traffic through the extracellular matrix is controlled by the membrane-anchored collagenase MT1-MMP (2004, background): “Indeed, tissueinfiltrating cancer cells of multiple origins have been noted to assume a mesenchymal cell-like phenotype similar to that displayed by fibroblasts (Thiery, 2002; Friedl and Wolf, 2003).”
• Chronic Inflammation and Cytokines in the Tumor Microenvironment (2014, background): “The mesenchymal phenotype provides increased motility that is associated with invasiveness and metastasis of tumor cells [138, 139].”
• Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “…quasi-mesenchymal cells that serve as the founders of metastatic colonies must be able to spawn large numbers of epithelial progeny to recreate the hierarchical relationships of CSCs and non-CSC that previously operated within the corresponding primary tumors (Malanchi et al., 2012; Thiery, 2002).”