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      Mesenchymal–epithelial transition (MET) as a mechanism for metastatic colonisation in breast cancer

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          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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          Author and article information

          Journal
          Cancer and Metastasis Reviews
          Cancer Metastasis Rev
          Springer Science and Business Media LLC
          0167-7659
          1573-7233
          December 2012
          June 23 2012
          December 2012
          : 31
          : 3-4
          : 469-478
          Article
          10.1007/s10555-012-9377-5
          22729277
          6a2f07ee-a457-4ec5-a06c-bce56deb4e8e
          © 2012

          http://www.springer.com/tdm

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