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Carcinogenesis Advance Access originally published online on May 25, 2009
Carcinogenesis 2009 30(7):1073-1081; doi:10.1093/carcin/bgp127
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability

Francesco Colotta1, Paola Allavena2, Antonio Sica2,3, Cecilia Garlanda2 and Alberto Mantovani2,4,*

1 Nerviano Medical Sciences, Nerviano, 20014 Nerviano, Milan, Italy
2 Department of Immunology and Inflammation, Istituto Clinico Humanitas IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy
3 Institute of Pathology, University of Piemonte Orientale, 28100 Novara, Italy
4 Department of Translational Medicine, University of Milan, 20121 Milan, Italy

* To whom correspondence should be addressed. Tel: +39 02 8224 2445; Fax: +39 02 8224 5101; Email: alberto.mantovani{at}humanitas.it

Inflammatory conditions in selected organs increase the risk of cancer. An inflammatory component is present also in the microenvironment of tumors that are not epidemiologically related to inflammation. Recent studies have begun to unravel molecular pathways linking inflammation and cancer. In the tumor microenvironment, smoldering inflammation contributes to proliferation and survival of malignant cells, angiogenesis, metastasis, subversion of adaptive immunity, reduced response to hormones and chemotherapeutic agents. Recent data suggest that an additional mechanism involved in cancer-related inflammation (CRI) is induction of genetic instability by inflammatory mediators, leading to accumulation of random genetic alterations in cancer cells. In a seminal contribution, Hanahan and Weinberg [(2000) Cell, 100, 57–70] identified the six hallmarks of cancer. We surmise that CRI represents the seventh hallmark.

Abbreviations: AID, activation-induced cytidine deaminase; BER, base excision repair; CI, chromosomal instability; CRI, cancer-related inflammation; DSB, double-strand break; HIF, hypoxia inducible factor; HR, homologous recombination; IL, interleukin; MDSC, myeloid-derived suppressor cell; MMP, matrix metalloproteinase; MMR, mismatch repair; MSI, microsatellite instability; NF-{kappa}B, nuclear factor-kappaB; NO, nitric oxide; ROS, reactive oxygen species; TAM, tumor-associated macrophage; TLR, toll-like receptor; TNF, tumor necrosis factor; UC, ulcerative colitis; VEGF, vascular endothelial growth factor

Received February 20, 2009; revised April 27, 2009; accepted May 14, 2009.


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