Title |
Mesenchymal–epithelial transition (MET) as a mechanism for metastatic colonisation in breast cancer
|
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Published in |
Cancer and Metastasis Reviews, June 2012
|
DOI | 10.1007/s10555-012-9377-5 |
Pubmed ID | |
Authors |
N. P. A. Devika Gunasinghe, Alan Wells, Erik W. Thompson, Honor J. Hugo |
Abstract |
As yet, there is no cure for metastatic breast cancer. Historically, considerable research effort has been concentrated on understanding the processes of metastasis, how a primary tumour locally invades and systemically disseminates using the phenotypic switching mechanism of epithelial to mesenchymal transition (EMT); however, much less is understood about how metastases are then formed. Breast cancer metastases often look (and may even function) as 'normal' breast tissue, a bizarre observation against the backdrop of the organ structure of the lung, liver, bone or brain. Mesenchymal to epithelial transition (MET), the opposite of EMT, has been proposed as a mechanism for establishment of the metastatic neoplasm, leading to questions such as: Can MET be clearly demonstrated in vivo? What factors cause this phenotypic switch within the cancer cell? Are these signals/factors derived from the metastatic site (soil) or expressed by the cancer cells themselves (seed)? How do the cancer cells then grow into a detectable secondary tumour and further disseminate? And finally--Can we design and develop therapies that may combat this dissemination switch? This review aims to address these important questions by evaluating long-standing paradigms and novel emerging concepts in the field of epithelial mesencyhmal plasticity. |
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Geographical breakdown
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France | 1 | <1% |
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Other | 1 | <1% |
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Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 83 | 27% |
Student > Master | 44 | 14% |
Student > Bachelor | 36 | 12% |
Researcher | 36 | 12% |
Student > Postgraduate | 17 | 5% |
Other | 34 | 11% |
Unknown | 60 | 19% |
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Chemistry | 5 | 2% |
Other | 30 | 10% |
Unknown | 71 | 23% |