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Upholding a role for EMT in breast cancer metastasis

AutorYe, Xin; Brabletz, Thomas; Kang, Yibin; Longmore, Gregory D.; Nieto, M. Ángela ; Stanger, Ben Z.; Yang, Jing; Weinberg, Robert A.
Fecha de publicación6-jul-2017
EditorSpringer Nature
CitaciónNature 547: E1-E6 (2017)
ResumenThe cell-biological program termed the epithelial-to-mesenchymal transition (EMT) has been invoked as a critical component of the metastatic process. Contrastingly, Fischer et al.1 recently reported that in two genetically engineered mouse models of mammary tumour development, carcinoma cells could metastasize without activating EMT programs. However, as detailed below, we find their evidence that EMT programs were not expressed in these primary tumours to be insufficient. Therefore, the contribution of EMT to carcinoma metastasis could not be ruled out in their analysis. There is a Reply to this Comment by Fischer, K. R. et al. Nature 547, 10.1038/nature22817 (2017).
Versión del editorhttp://dx.doi.org/10.1038/nature22816
URIhttp://hdl.handle.net/10261/167803
DOI10.1038/nature22816
ISSN0028-0836
1476-4687
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