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Open AccessJournal ArticleDOI

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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Twist2 contributes to breast cancer progression by promoting an epithelial-mesenchymal transition and cancer stem-like cell self-renewal.

TL;DR: The overexpression of Twist2 may contribute to breast cancer progression by activating the EMT programme and enhancing the self-renewal of cancer stem-like cells.
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Twist1-induced dissemination preserves epithelial identity and requires E-cadherin

TL;DR: Expression of the transcription factor Twist1 induces dissemination of normal mammary epithelial cells without changing the RNA levels of epithelial-specific genes such as E-cadherin.
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Non-small cell lung cancer cells survived ionizing radiation treatment display cancer stem cell and epithelial-mesenchymal transition phenotypes

TL;DR: It is suggested that radiation survived cells have a complex phenotype combining the properties of CSCs and EMT, and might be considered as markers of radiotherapy response in NSCLC.
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TGF-β drives epithelial-mesenchymal transition through δEF1-mediated downregulation of ESRP

TL;DR: A microarray-based analysis at single exon level found that TGF-β induces broad alteration of splicing patterns by downregulating epithelial splicing regulatory proteins (ESRPs), and δEF1 family proteins repress the expression of ESRPs to regulate alternative splicing during T GF-β-induced EMT and the progression of breast cancers.
References
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Journal ArticleDOI

Gene expression profiling predicts clinical outcome of breast cancer

TL;DR: DNA microarray analysis on primary breast tumours of 117 young patients is used and supervised classification is applied to identify a gene expression signature strongly predictive of a short interval to distant metastases (‘poor prognosis’ signature) in patients without tumour cells in local lymph nodes at diagnosis, providing a strategy to select patients who would benefit from adjuvant therapy.
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Epithelial–mesenchymal transitions in tumour progression

TL;DR: Epithelial–mesenchymal transition provides a new basis for understanding the progression of carcinoma towards dedifferentiated and more malignant states.
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New functions for the matrix metalloproteinases in cancer progression

TL;DR: It is shown that the MMPs have functions other than promotion of invasion, have substrates other than components of the extracellular matrix, and that they function before invasion in the development of cancer.
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Involvement of chemokine receptors in breast cancer metastasis.

TL;DR: It is reported that the chemokine receptors CXCR4 and CCR7 are highly expressed in human breast cancer cells, malignant breast tumours and metastases and their respective ligands CXCL12/SDF-1α and CCL21/6Ckine exhibit peak levels of expression in organs representing the first destinations of breast cancer metastasis.
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The pathogenesis of cancer metastasis: the 'seed and soil' hypothesis revisited

TL;DR: It is now known that the potential of a tumour cell to metastasize depends on its interactions with the homeostatic factors that promote tumour-cell growth, survival, angiogenesis, invasion and metastasis.
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