Mesenchymal-epithelial transition (MET) as a mechanism for metastatic colonisation in breast cancer
Gunasinghe, N.P.A. Devika, Wells, Alan, Thompson, Erik W., & Hugo, Honor J. (2012) Mesenchymal-epithelial transition (MET) as a mechanism for metastatic colonisation in breast cancer. Cancer and Metastasis Reviews, 31(3-4), pp. 469-478.
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 finallyCan 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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|Item Type:||Journal Article|
|Additional Information:||Cited By (since 1996):29
Export Date: 6 May 2014
PubMed ID: 22729277
|Keywords:||Breast cancer, EMT, Epithelial, Mesenchymal, MET, Metastasis, Proliferation, Transition|
|Divisions:||Current > QUT Faculties and Divisions > Faculty of Health|
|Deposited On:||29 May 2014 02:48|
|Last Modified:||29 Aug 2016 07:36|
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