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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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Epithelial-mesenchymal transition as a fundamental underlying pathogenic process in COPD airways: fibrosis, remodeling and cancer

TL;DR: The current literature on EMT and the relative expression of specific TF activity is reviewed, to define the networks likely to be involved in a similar process in the airways of patients with smoking-related COPD.
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Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis *♦

TL;DR: The findings suggest that hyaluronan overproduction allows plastic cancer cell populations to revert to stem cell states via Twist and the TGF-β-Snail signaling axis.
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Suppression of Invasion and Metastasis of Triple-Negative Breast Cancer Lines by Pharmacological or Genetic Inhibition of Slug Activity

TL;DR: It is shown here that PCPA treatment induces the expression of E-cadherin and other epithelial markers and markedly suppresses migration and invasion of TNBC cell lines MDA-MB-231 and BT-549, and blocking Slug activity may suppress the metastatic spread of T NBC and, perhaps, specifically inhibit homing/colonization to the bone.
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Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas.

TL;DR: Deletions at TWIST were statistically correlated to other molecular abnormalities, like alterations at the APC or c‐kit loci, as well as to clinical features such as a poor outcome, shows that the TWIST gene seemed to be involved in high‐grade pediatric osteosarcomas and is a new marker with a possible initial predictive value.
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DNA damage response regulation by microRNAs as a therapeutic target in cancer

TL;DR: The therapeutic importance of miRNAs in modulation of DDR/DNA repair mechanisms will be discussed and a brief introduction about miRNA biogenesis and functions, DDR pathways, and recent findings about DDR-microRNA interactions are provided.
References
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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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