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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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Epithelial‐mesenchymal Transition and Cancer Stem Cells: At the Crossroads of Differentiation and Dedifferentiation

TL;DR: This review explores the connections between epithelial‐mesenchymal transition (EMT) and differentiation status and suggests that EMT brings about dedifferentiation that enables subsequent differentiation.
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Gap junction as an intercellular glue: Emerging roles in cancer EMT and metastasis

TL;DR: GJ serves as an intercellular glue to suppress EMT and cancer metastasis and there are signs that GJs contribute to cell adhesion and migration (the pathological feature of EMT) in breast cancer.
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Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression.

TL;DR: Using the MCF-10A-series of cell lines that recapitulate the early stages of breast cancer formation and EMT, it is found that TWIST1 to be upregulated during EMT and downregulated early in carcinogenesis and that miR-580, CPEB1, and C PEB2 act as negative regulators of TWist1 expression in a sequence-specific and additive/cooperative manner.
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An in vitro correlation of mechanical forces and metastatic capacity

TL;DR: It is concluded that traction stress, adhesion strength and rate of migration do indeed change as tumor cells progress in metastatic capacity and do so in a dimension-sensitive manner.
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AP-2α and AP-2γ regulate tumor progression via specific genetic programs

TL;DR: It is shown that increased xeno‐transplant growth was mostly due to highly enhanced proliferation of the tumor cells together with reduced innate immune cell recruitment, and it was showed that migration impairment was mediated, at least in part, by secreted factors.
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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