Immunosuppression associated with chronic inflammation in the tumor microenvironment
- PMID: 26354776
- PMCID: PMC5006153
- DOI: 10.1093/carcin/bgv123
Immunosuppression associated with chronic inflammation in the tumor microenvironment
Abstract
Chronic inflammation contributes to cancer development via multiple mechanisms. One potential mechanism is that chronic inflammation can generate an immunosuppressive microenvironment that allows advantages for tumor formation and progression. The immunosuppressive environment in certain chronic inflammatory diseases and solid cancers is characterized by accumulation of proinflammatory mediators, infiltration of immune suppressor cells and activation of immune checkpoint pathways in effector T cells. In this review, we highlight recent advances in our understanding of how immunosuppression contributes to cancer and how proinflammatory mediators induce the immunosuppressive microenvironment via induction of immunosuppressive cells and activation of immune checkpoint pathways.
© The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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References
- 
    - Kuper H., et al. (2000) Infections as a major preventable cause of human cancer. J. Intern. Med., 248, 171–183. - PubMed
 
- 
    - Algra A.M., et al. (2012) Effects of regular aspirin on long-term cancer incidence and metastasis: a systematic comparison of evidence from observational studies versus randomised trials. Lancet Oncol., 13, 518–527. - PubMed
 
- 
    - Harris R.E. (2009) Cyclooxygenase-2 (cox-2) blockade in the chemoprevention of cancers of the colon, breast, prostate, and lung. Inflammopharmacology, 17, 55–67. - PubMed
 
- 
    - Rothwell P.M., et al. (2012) Short-term effects of daily aspirin on cancer incidence, mortality, and non-vascular death: analysis of the time course of risks and benefits in 51 randomised controlled trials. Lancet, 379, 1602–1612. - PubMed
 
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