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Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways

Chronic inflammation and infection are major causes of cancer. There are continued improvements to our understanding of the molecular connections between inflammation and cancer. Key mediators of inflammation-induced cancer include nuclear factor kappa B, reactive oxygen and nitrogen species, inflam...

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Published in:Carcinogenesis (New York) 2010-01, Vol.31 (1), p.37-49
Main Authors: Schetter, Aaron J., Heegaard, Niels H. H., Harris, Curtis C.
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Language:English
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description Chronic inflammation and infection are major causes of cancer. There are continued improvements to our understanding of the molecular connections between inflammation and cancer. Key mediators of inflammation-induced cancer include nuclear factor kappa B, reactive oxygen and nitrogen species, inflammatory cytokines, prostaglandins and specific microRNAs. The collective activity of these mediators is largely responsible for either a pro-tumorigenic or anti-tumorigenic inflammatory response through changes in cell proliferation, cell death, cellular senescence, DNA mutation rates, DNA methylation and angiogenesis. As our understanding grows, inflammatory mediators will provide opportunities to develop novel diagnostic and therapeutic strategies. In this review, we provide a general overview of the connection between inflammation, microRNAs and cancer and highlight how our improved understanding of these connections may provide novel preventive, diagnostic and therapeutic strategies to reduce the health burden of cancer.
doi_str_mv 10.1093/carcin/bgp272
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subjects Animals
Biological and medical sciences
Cancer Biology
Carcinogenesis, carcinogens and anticarcinogens
Cytokines - metabolism
Free Radicals - metabolism
Humans
Inflammation - genetics
Inflammation - metabolism
Medical sciences
MicroRNAs - genetics
Neoplasms - genetics
Neoplasms - metabolism
Tumor Suppressor Protein p53 - metabolism
Tumors
title Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways
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