File:Schematic representation of various mechanisms that have been reported to regulate epithelial–mesenchymal transition (EMT) in SACC patients.png
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| Description | Figure 2. Schematic representation of various mechanisms that have been reported to regulate epithelial–mesenchymal transition (EMT) in SACC (Salivary adenoid cystic carcinoma) patients. Five distinct regulatory mechanisms have been identified, including hypoxia, the activation of growth factors and developmental pathways (such as the transforming growth factor ß (TGF-ß) and Wnt signaling pathway), interaction between cancer-associated fibroblasts and adjacent tumor cells, and genomic or epigenomic alterations (such as MYB-NFIB fusion, p53 mutation, and microRNA (miR) expression). These factors play a significant role in the modulation of the epithelial–mesenchymal spectrum. VEGF: vascular endothelial growth factor; EGF: epidermal growth factor; FGF: fibroblast growth factor; PDGF: platelet-derived growth factor; HGF: hepatocyte growth factor; RTK: receptor tyrosine kinase; mTOR: mammalian target of rapamycin; GSK3β: glycogen synthase kinase-3 beta; CK1a: casein kinase 1a; APC: adenomatous polyposis coli; LEF: lymphoid enhancer-binding factor; TCF: T cell factors; HIF1α: hypoxia-inducible factor 1-alpha. (Figure created using BioRender, Toronto, ON, Canada). |
| Date | |
| Source | https://www.mdpi.com/2072-6694/15/11/2886 Unraveling the Role of Epithelial–Mesenchymal Transition in Adenoid Cystic Carcinoma of the Salivary Glands: A Comprehensive Review. Cancers 2023, 15, 2886. https://doi.org/10.3390/cancers15112886 |
| Author | Hoch, C.C.; Stögbauer, F.; Wollenberg, B. |
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| current | 09:56, 30 May 2024 | | 3,971 × 3,326 (3.15 MB) | Rasbak (talk | contribs) | {{Information |description=Figure 2. Schematic representation of various mechanisms that have been reported to regulate epithelial–mesenchymal transition (EMT) in SACC patients. Five distinct regulatory mechanisms have been identified, including hypoxia, the activation of growth factors and developmental pathways (such as the transforming growth factor ß (TGF-ß) and Wnt signaling pathway), interaction between cancer-associated fibroblasts and adjacent tumor cells, and genomic or epigenomic al... |
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