Journal
CLINICAL CANCER RESEARCH
Volume 19, Issue 11, Pages 2810-2816Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1078-0432.CCR-12-1961
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Funding
- European Research Council Advanced Investigator Grant [ERC-2011-AdG294464]
- Greek Operational Program Education and Lifelong Learning of the National Strategic Reference Framework (NSRF), Thales [Thales 656]
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Inflammatory signals from the surrounding microenvironment play important roles in tumor promotion. Key inflammatory mediators and pathways that induce and sustain tumorigenesis have recently been identified in many different cancers. Hepatocellular carcinoma is a paradigm for inflammation-induced cancer, as it most frequently develops in the setting of chronic hepatitis, consecutive cellular damage, and compensatory regeneration. Recent studies revealed that liver damage-mediated inflammation and carcinogenesis are triggered by a complex cross-talk between NF-kappa B, c-jun-NH2-kinase, and STAT3 signaling pathways. Molecular dissection of the mechanisms involved in the interplay between these pathways identified promising new targets for therapeutic intervention. Targeting different components of the signaling cascades may provide efficient means for blocking the apparently irreversible sequence of events initiated by chronic liver inflammation and culminating in liver cancer. (C) 2013 AACR.
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