TGF-β and epithelial-to-mesenchymal transitions

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Visualizing stromal cell dynamics in different tumor microenvironments by spinning disk confocal microscopy (2008, background): “Recent reports in various cellular models have documented a role for MAPKs, particularly ERKs, in the establishment of EMT (Zavadil and Bottinger, 2005).”
Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets (2006, background): “Recently, epithelial to mesenchymal transition (EMT) has been suggested in some fibrotic organs as an important pathogenetic pathway to increase the number of fibrogenic cells [36, 37].”
Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “TGF-b is one of the more robust cues inducing EMT in different model systems (reviewed by Zavadil and Bottinger, 2005), leading to the upregulation of several EMT inducers, including SNAI1/SNAI2, ZEB1, Twist and the Id factors through Smad-dependent and Smad-independent pathways (Peinado et al.,…”
Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer. (2006, background): “…(Solcia et al. 1995; Hruban et al. 2006)—and Smad4/TGF- signaling has been implicated in processes of epithelial differentiation (for review, see Zavadil and Bottinger 2005), we sought to determine whether Smad4 status influenced the morphological presentation of the Cre LSL-KrasG12D…”