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Twist, a Master Regulator of Morphogenesis, Plays an Essential Role in Tumor Metastasis

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TLDR
A mechanistic link between Twist, EMT, and tumor metastasis is established, suggesting that Twist contributes to metastasis by promoting an epithelial-mesenchymal transition (EMT).
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This article is published in Cell.The article was published on 2004-06-25 and is currently open access. It has received 3670 citations till now. The article focuses on the topics: Twist transcription factor & Metastasis.

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The basics of epithelial-mesenchymal transition

TL;DR: 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.
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The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells

TL;DR: It is reported that the induction of an EMT in immortalized human mammary epithelial cells (HMLEs) results in the acquisition of mesenchymal traits and in the expression of stem-cell markers, and it is shown that those cells have an increased ability to form mammospheres, a property associated with mammARY epithelial stem cells.
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Cancer Metastasis: Building a Framework

TL;DR: Understanding of the origins and nature of cancer metastasis and the selection of traits that are advantageous to cancer cells is promoted.
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Complex networks orchestrate epithelial–mesenchymal transitions

TL;DR: Understanding how mesenchymal cells arise from an epithelial default status will also have a strong impact in unravelling the mechanisms that control fibrosis and cancer progression.
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The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1.

TL;DR: It is found that all five members of the microRNA-200 family were markedly downregulated in cells that had undergone EMT in response to transforming growth factor (TGF)-β or to ectopic expression of the protein tyrosine phosphatase Pez, suggesting that downregulation of themicroRNAs may be an important step in tumour progression.
References
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Multiple ways of silencing E-cadherin gene expression in lobular carcinoma of the breast.

TL;DR: It is concluded that most ILCs show genetic or epigenetic changes affecting the E‐cadherin gene and that many of these tumours lack E‐ cadher in expression, consistent with biallelic inactivation of CDH1 by promoter methylation, mutation or allelic loss in any combination.
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Twist function is required for the morphogenesis of the cephalic neural tube and the differentiation of the cranial neural crest cells in the mouse embryo.

TL;DR: Cell transplantation studies reveal that Twist activity is required in the cranial mesenchyme for directing the migration of the neural crest cells, as well as in the Neural crest cells within the first branchial arch to achieve correct localization.
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Twist Protein in Mouse Embryogenesis

TL;DR: A proposed role of MTwist in somite formation and maturation is inhibition of myogenic bHLH and MEF2 genes and thus prevention of premature and/or ectopic differentiation in the presomitic mesoderm and epithelial somites.
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Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer.

TL;DR: It is concluded that LOH at 16q is the most frequent chromosome alteration and E-cadherin is a typical tumour suppressor gene in lobular breast cancer.
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Epithelium-mesenchyme interconversion as example of epithelial plasticity

TL;DR: In vitro studies indicate that growth factors, growth‐factor related molecules and extracellular matrix components are involved in initiation of EMT, and the cellular targets of E MT‐inducing molecules are likely to include molecules participating in cell adhesion systems.
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