Aging, inflammation and cancer

Barbara Bottazzi; Elio Riboli; Alberto Mantovani

doi:10.1016/j.smim.2018.10.011

Aging, inflammation and cancer

Semin Immunol. 2018 Dec:40:74-82. doi: 10.1016/j.smim.2018.10.011. Epub 2018 Nov 6.

Authors

Barbara Bottazzi¹, Elio Riboli², Alberto Mantovani³

Affiliations

¹ Humanitas Clinical and Research Center, via Manzoni 56, 20089, Rozzano, Milan, Italy.
² Humanitas University, via Rita Levi Montalcini, 20090, Pieve Emanuele, Milan, Italy; School of Public Health, Imperial College London, London, UK.
³ Humanitas Clinical and Research Center, via Manzoni 56, 20089, Rozzano, Milan, Italy; Humanitas University, via Rita Levi Montalcini, 20090, Pieve Emanuele, Milan, Italy; The William Harvey Research Institute, Queen Mary University of London, London, UK. Electronic address: alberto.mantovani@humanitasresearch.it.

PMID: 30409538
DOI: 10.1016/j.smim.2018.10.011

Abstract

Aging is a key aspect of neoplasia at the level of cells, individuals and populations. Unrestrained expression and production of inflammatory mediators is a key feature of aging at the cellular and organism level. Inflammatory cells and mediators are a key component of the tumor microenvironment and drive tumor progression. Non-resolving smoldering inflammation increases the risk of cancer (the extrinsic pathway connecting inflammation and cancer). In the intrinsic pathway, genetic events that cause neoplasia (oncogenes and oncosupressor genes) orchestrate the construction of cancer-related inflammation. We argue that uncontrolled smoldering inflammation drives carcinogenesis in aging and acts as a common denominator linking aging and cancer.

Keywords: Cancer; Immunosenescence; Inflammaging.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Aging*
Animals
Carcinogenesis
Cellular Senescence
Humans
Inflammation*
Neoplasms / immunology*
Oncogenes / genetics
Tumor Microenvironment
Tumor Suppressor Proteins / metabolism

Substances

Tumor Suppressor Proteins