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

Carcinogenesis · 2009 · Vol. 31(1) · pp. 37–49
Aaron J. SchetterNiels H. H. HeegaardCurtis C. Harris

Abstract

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.

MicroRNA in disease regulationCancer-related molecular mechanisms researchCircular RNAs in diseasesInflammationCancermicroRNAAngiogenesisCancer researchCytokineCarcinogenesisDNA damageDNA methylationImmunology

MeSH terms

AnimalsFree RadicalsHumansInflammationNeoplasmsTumor Suppressor Protein p53CytokinesMicroRNAs

Funding

  • National Institutes of Health
  • National Cancer Institute
Citations
651
FWCI
16.38
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References
193
Percentile
99%
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