Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression

By Honor J. Hugo, M. Ackland, T. Blick, M. Lawrence, J. Clements, E. Williams, Erik W. Thompson. Journal of Cellular Physiology, 2007

1,136 citations recorded by the source corpus.

Subfields: Oncology

View Paper: https://www.semanticscholar.org/paper/7a10a4f334fd2881871c9cdd10d53b8968d479d6

How researchers see this paper

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

In Oncology

1. Jing Yang
2. R. Weinberg
3. Thomas Brabletz
4. M. Nieto
5. G. Moreno-Bueno
6. J. Tsai
7. J. Palacios
8. D. Sarrió

Citations in the corpus

• Epithelial-mesenchymal transition in breast cancer relates to the basal-like phenotype. (2008, background): “In addition, stem cell–like breast cell lines (e.g., MCF10A and PMC42-LA) are able to undergo EMT ( 36 ).”
• Hallmarks of cancer: the next generation. (2011, neutral): “This plasticity may result in the formation of new tumor colonies of carcinoma cells exhibiting a histopathology similar to those of carcinoma cells in the primary tumor that never underwent an EMT (Hugo et al., 2007).”
• EMT, MET, plasticity and tumor metastasis (2020, background): “In summary, a substantial amount of research investigating breast, ovarian and pancreatic cancers suggests the importance of MET [67].”
• A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells (2008, background): “EMBO open A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells”
• Spatiotemporal regulation of epithelial-mesenchymal transition is essential for squamous cell carcinoma metastasis. (2012, result): “Our study, together with other clinical studies in breast, ovarian, and prostate cancers (Chao et al., 2010; Hudson et al., 2008; Hugo et al., 2007), indicates that EMT is activated in many types of primary human carcinoma, but not in their distant metastases.”
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “In parallel, transcription factors implicated in the down-regulation of the epithelial E-cadherin and widely used as markers for EMT like SNAIL1, SNAIL2, Twist, EF1/ZEB1 and SIP1/ZEB2 have been associatedwith the cancer invasive front [75,172].”
• Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “Importantly, the heightened metastatic potential of such clusters as compared to that of the same numbers of individual cells was recognized (117, 118) even before EMT was characterized as a metastasis mechanism (119).”