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The basics of epithelial-mesenchymal transition

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TLDR
Processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias and the identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes.
Abstract
The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

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Immunity, Inflammation, and Cancer

TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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The Molecular Signatures Database Hallmark Gene Set Collection

TL;DR: A combination of automated approaches and expert curation is used to develop a collection of "hallmark" gene sets, derived from multiple "founder" sets, that conveys a specific biological state or process and displays coherent expression in MSigDB.
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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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Matrix Metalloproteinases: Regulators of the Tumor Microenvironment

TL;DR: In addition to their role in extracellular matrix turnover and cancer cell migration, MMPs regulate signaling pathways that control cell growth, inflammation, or angiogenesis and may even work in a nonproteolytic manner.
References
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Activation of an inducible c-FosER fusion protein causes loss of epithelial polarity and triggers epithelial-fibroblastoid cell conversion.

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Disruption of tissue-type plasminogen activator gene in mice reduces renal interstitial fibrosis in obstructive nephropathy

TL;DR: It is demonstrated that ablation of tPA attenuated renal interstitial fibrotic lesions in obstructive nephropathy and established a crucial and definite importance of EMT in the pathogenesis of renal interinterstitial fibrosis at the whole-animal level.
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Posteriorization by FGF, Wnt, and retinoic acid is required for neural crest induction.

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Journal Article

Snail is required for TGFβ-induced endothelial-mesenchymal transition of embryonic stem cell-derived endothelial cells

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The Spemann organizer gene, Goosecoid, promotes tumor metastasis

TL;DR: It is demonstrated that Goosecoid promotes tumor cell malignancy and suggested that other conserved organizer genes may function similarly in human cancer.
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