S
Samy Lamouille
Researcher at Virginia Tech
Publications - 26
Citations - 11537
Samy Lamouille is an academic researcher from Virginia Tech. The author has contributed to research in topics: Epithelial–mesenchymal transition & Cancer. The author has an hindex of 17, co-authored 23 publications receiving 9656 citations. Previous affiliations of Samy Lamouille include Joseph Fourier University & French Alternative Energies and Atomic Energy Commission.
Papers
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Molecular mechanisms of epithelial–mesenchymal transition
TL;DR: The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues, and the convergence of signalling pathways is essential for EMT.
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TGF-beta-induced epithelial to mesenchymal transition.
TL;DR: The induction of EMT in response to TGF-β is discussed, and the underlying signaling and transcription mechanisms are focused on.
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TGF-β signaling and epithelial-mesenchymal transition in cancer progression.
TL;DR: The differentiation plasticity of epithelial cells that mediates TGF-&bgr;-induced EMT and reversion from mesenchymal to epithelial phenotype are increasingly seen as integral aspects of cancer progression that contribute to survival and dissemination of cancer cells.
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Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells
Deepa Subramanyam,Samy Lamouille,Robert L. Judson,Jason Liu,Nathan Bucay,Rik Derynck,Robert Blelloch +6 more
TL;DR: It is demonstrated that the human ESCC miRNAs promote dedifferentiation by acting on multiple downstream pathways, and it is proposed that individual mi RNAs generally act through numerous pathways that synergize to regulate and enforce cell fate decisions.
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Cell size and invasion in TGF-β–induced epithelial to mesenchymal transition is regulated by activation of the mTOR pathway
Samy Lamouille,Rik Derynck +1 more
TL;DR: Activation of mTOR by TGF-β, which leads to increased cell size and invasion, adds to the role of T GF-β–induced EMT in cancer progression and may represent a therapeutic opportunity for rapamycin analogues in cancer.