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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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Carbonic anhydrase IX (CA9) modulates tumor-associated cell migration and invasion

TL;DR: The results suggest that CA9 overexpression induces weakening of cell adhesions and augmented cell motility by aberrant Rho-GTPase signal transduction by showing an underlying mechanism of CA9-related enhanced metastatic potential of tumor cells.
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A Perspective on the Development of TGF-β Inhibitors for Cancer Treatment.

TL;DR: The rationale and challenges of targeting TGF-β signaling in cancer are discussed, the clinical status of TGF -β signaling inhibitors that interfere with TGF−β bioavailability, TGF+β/receptor interaction, or T GF-β receptor kinase function are summarized, and alternative approaches by using promising technologies are discussed.
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Tinagl1 Suppresses Triple-Negative Breast Cancer Progression and Metastasis by Simultaneously Inhibiting Integrin/FAK and EGFR Signaling.

TL;DR: E ectopic expression and therapeutic delivery of the secreted protein Tubulointerstitial nephritis antigen-like 1 (Tinagl1) suppresses TNBC progression and metastasis through direct binding to integrin α5β1, αv β1, and epidermal growth factor receptor (EGFR), and subsequent simultaneous inhibition of focal adhesion kinase (FAK) and EGFR signaling pathways.
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Epithelial-to-mesenchymal transition predicts prognosis of pancreatic cancer

TL;DR: EMT status is an important prognostic factor for pancreatic cancer and is associated with portal vein invasion and lymph node metastasis.
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Overexpression of cathepsin Z contributes to tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma

TL;DR: Functional study found that CTSZ could increase colony formation in soft agar and promote cell motility and the metastatic effect of C TSZ was associated with its role in inducing epithelial-mesenchymal transition (EMT), which played an important role in HCC metastasis.
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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