The basics of epithelial-mesenchymal transition.
By Raghu Kalluri, R. Weinberg. Journal of Clinical Investigation, 2009
5,284 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/49bc7cb0f67a8d86b55dc82dacb2cb398515f8c0
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Citations in the corpus
- Role of interleukin-6 in cancer progression and therapeutic resistance (2016, background): “known as the epithelial-to-mesenchymal transition (EMT) and its counterpart, the mesenchymal-to-epithelial transition [139].”
- IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis. (2014, background): “Therefore, we hypothesized that the downregulation of IL6R expression by miR-34a may contribute to MET mediated by p53.”
- Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Y. Shintani, M. A. Hollingsworth, M. J. Wheelock, K. R. Johnson, Collagen I promotes metastasis in pancreatic cancer by activating c-Jun NH2-terminal kinase 1 and up-regulating N-cadherin expression.”
- Immunity, Inflammation, and Cancer (2010, background): “The first step is represented by epithelial-mesenchymal transition, in which cancer cells acquire fibroblastoid characteristics that increase their motility and allow them to invade epithelial linings/basal membranes and reach efferent blood vessels or lymphatics (Kalluri and Weinberg, 2009).”
- Spatiotemporal regulation of epithelial-mesenchymal transition is essential for squamous cell carcinoma metastasis. (2012, background): “Studies using cell culture and tumor xenograft models show that activation of EMT promotes carcinoma cells to dissociate from each other and metastasize to distant organs (Hay, 1995; Kalluri and Weinberg, 2009; Thiery, 2002, 2009).”
- The EMT-activator Zeb1 is a key factor for cell plasticity and promotes metastasis in pancreatic cancer (2017, neutral): “Scoring for CD31 and Gata6 was done according to staining intensity, with no (0), low (1), medium (2) and high (3) expression.”
- TGF-β/SMAD Pathway and Its Regulation in Hepatic Fibrosis (2016, background): “Vimentin is a well-recognized marker for EMT, as is E-cadherin for epithelial cells (Kalluri and Weinberg 2009).”
- The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “However, the EMTs associated with organ fibrosis are not plastic: The disease progresses so that the organs are finally mainly composed of activated fibroblastic and fibrogenic cells that lead to organ failure.”
- Inertial Focusing for Tumor Antigen–Dependent and –Independent Sorting of Rare Circulating Tumor Cells (2013, background): “CTC analysis of three patients whose cancer lacks the translocation was used to establish specificity: a prostate cancer patient (lane 1), an EGFR mutant lung cancer patient (lane 2), and a HER2-amplified lung cancer patient (lane 6). ienceTranslationalMedicine.org 3 April 2013 Vol 5 Issue 179 179ra”
- Cellular and molecular mechanisms of renal fibrosis (2011, background): “Epithelial–mesenchymal transition Another source of matrix-producing cells could be tubular epithelium that undergoes EMT, a cell phenotypic conversion process that occurs during embryonic development, tumor metastasis and organ fibrosis”