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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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Journal Article

E-cadherin is inactivated in a majority of invasive human lobular breast cancers by truncation mutations throughout its extracellular domain.

TL;DR: Evidence is provided that frequent E-cadherin mutations are involved in the particular etiology of sporadic lobular breast cancers and in 0 of 50 breast cancers of other histopathological subtypes.
Journal Article

Differential loss of E-cadherin expression in infiltrating ductal and lobular breast carcinomas.

TL;DR: The data indicate that loss of E-cadherin expression is an early event in the formation of the lobular type of breast carcinomas and may account for the extended spread of lobular carcinoma in situ and the peculiar diffuse invasion mode of ILC.
Journal Article

Correlation of E-cadherin expression with differentiation grade and histological type in breast carcinoma.

TL;DR: Results indicate that E-CD expression correlates with histological type and grade in breast carcinomas and positively with the degree of tubular formation and inversely with the mitoses number.
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dorsal-twist interactions establish snail expression in the presumptive mesoderm of the Drosophila embryo.

TL;DR: Evidence that dl and twi directly activate sna expression is presented, consistent with the possibility that the sharp sna borders are formed by multiplying the shallow dl gradient and the steeper twi gradient.
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The twist gene: isolation of a Drosophila zygotic gene necessary for the establishment of dorsoventral pattern.

TL;DR: The twist zygotic gene appears to be involved in the establishment of the dorso-ventral pattern in Drosophila embryos, and it is determined the temperature-sensitive period of twist around the gastrulation time, and the gene is isolated.
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