Intersecting pathways in inflammation and cancer: Hepatocellular carcinoma as a paradigm

doi:10.5306/wjco.v3.i2.15

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Feb 10, 2012 (publication date) through Jan 10, 2025

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World Journal of Clinical Oncology

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2218-4333

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Clin Oncol. Feb 10, 2012; 3(2): 15-23
Published online Feb 10, 2012. doi: 10.5306/wjco.v3.i2.15

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Figure 1 The intrinsic and extrinsic pathways combine to create a local microenvironment around the injured and transformed hepatocyte to augment tumor promoting mechanisms. ROS: Reactive oxygen species; HIF1α: Hypoxia inducible factor 1 alpha; NK cell: Natural killer cell; MDSC: Myeloid derived suppressor cell; IL: Interleukin; TGF-β: Transforming growth factor Beta; HGF: Hepatocyte growth factor; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; CXCL: Chemokine ligand; STAT3: Signal transducer and activator of transcription 3.

Citation: Wai PY, Kuo PC. Intersecting pathways in inflammation and cancer: Hepatocellular carcinoma as a paradigm. World J Clin Oncol 2012; 3(2): 15-23
URL: https://www.wjgnet.com/2218-4333/full/v3/i2/15.htm
DOI: https://dx.doi.org/10.5306/wjco.v3.i2.15