Epithelial-mesenchymal transitions in development and disease.
By J. P. Thiery, H. Acloque, R. Huang, M. Nieto. Cell, 2009
9,583 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/389ac3e28f10660aea3a40bd802473e3e9ef3407
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Citations in the corpus
- The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “…of the TGF-β superfamily: Wnts, Notch, epithelial growth factor (EGF), hepatocyte growth factor (HGF), fibroblast growth factor (FGF), hypoxia-inducible factor (HIF), Sonic hedgehog (Shh), and others (as discussed in detail in excellent reviews, e.g., De Craene et al. 2005, Thiery & Sleeman 2006).”
- Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast (2011, background): “An array of contextual signals has been implicated in the induction of an EMT, almost invariably in cells that have undergone unknown predisposing genetic changes (Thiery et al., 2009).”
- Targeting cancer stem cells by inhibiting Wnt, Notch, and Hedgehog pathways (2011, background): “This multi-step process results in the loss of cell-to-cell adhesive properties, loss of cell polarity, and the gain of invasive and migratory mesenchymal properties”
- Management of acquired resistance to EGFR TKI–targeted therapy in advanced non-small cell lung cancer (2018, neutral): “Different EMT transcription factors, including Slug, ZEB1, Snail, and AXL, changed with the development of acquired resistance to EGFR TKIs [42, 44].”
- Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization (2011, background): “2401" language="eng" relation="no"> Early events of metastatic dissemination are thought to be initiated by epithelial-to-mesenchymal transition (EMT) in carcinoma cells, promoting tumor cell migration and invasio”
- The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “Tissue regeneration is associated with organ fibrosis and disease progression and ultimately causes organ failure [21].”
- Loss of FBP1 by Snail-mediated Repression Provides Metabolic Advantages in Basal-like Breast Cancer (2013, neutral): “The increased motility and invasiveness of metastatic tumor cells are reminiscent of the events that occur at the epithelial-mesenchymal transition (EMT), a characteristic of embryonic development, tissue remodeling and wound healing (Polyak and Weinberg, 2009; Thiery et al., 2009).”
- The Roles of Autophagy in Cancer (2018, background): “These processes induce metastasis of cancer, leading to a lack of cell-cell adhesion, cell polarity to increase of cell motility, polarity, and invasiveness [111,112].”
- Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged. (2010, background): “In addition, a process that often plays a role in the acquisition of invasive behavior in cancer cells, the epithelial-to-mesenchymal transition (EMT), is accompanied by a reprogramming of AS (Thiery et al. 2009).”
- The Hippo pathway: regulators and regulations. (2013, background): “YAP and TAZ induced an epithelial–mesenchymal transition (EMT), a phenomenon crucial for the initiation of cancer metastasis (Overholtzer et al. 2006; Lei et al. 2008; Thiery et al. 2009).”
- Distinct EMT programs control normal mammary stem cells and tumour-initiating cells (2015, neutral): “Indeed, Snail had been reported to activate Zeb1 expression in non-mammary types of epithelial cells 29,30 .”
- IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis. (2014, background): “org Volume 124 Number 4 April 2014 ses (3, 42).”
- TGF-β1 Signaling and Tissue Fibrosis. (2018, background): “More insight has emerged with greater usage of fibrotic human tissue samples for biomedical research, the development of novel techniques for genetic modifications to mice, and a greater understanding of some of the prominent EMT signaling pathways (Kalluri and Neilson 2003; Teng et al. 2007; Kallur”