title: Cancer and inflammation.
abstract: The relationship between inflammation and cancer has been recognized since the 17thcentury,1and we now know much about the cells, cytokines and physiological processes that are central to both inflammation and cancer.2-9Chronic inflammation can induce certain cancers,10-17and solid tumors, in turn, can initiate and perpetuate local inflammatory processes that foster tumor growth and dissemination.5,18-20Consequently, inflammatory pathways have been targeted in attempts to control cancer.21-23Inflammation is a central aspect of the innate immune system's response to tissue damage or infection, and also facilitates the recruitment of circulating cells and antibodies of the adaptive immune response to the tissue. Components of the innate immune response carry out a robust, but sometimes overly-conservative response, sacrificing specificity for the sake of preservation. Thus, when innate immunity goes awry, it can have profound implications. How the innate and adaptive immune systems cooperate to neutralize pathogens and repair damaged tissues is still an area of intense investigation. Further, how these systems can respond to cancer, which arises from normal 'self' cells that undergo an oncogenic transformation, has profound implications for cancer therapy. Recently, immunotherapies that activate adaptive immunity have shown unprecedented promise in the clinic, producing durable responses and dramatic increases in survival rate in patients with advanced stage melanoma.24-26Consequently, the relationship between cancer and inflammation has now returned to the forefront of clinical oncology. WIREs Syst Biol Med 2017, 9:e1370. doi: 10.1002/wsbm.1370 For further resources related to this article, please visit the WIREs website.
authors.affiliation: Department of Radiation Oncology, Massachusetts General Hospital, Boston, MA, USA.
authors.forename: Lance L
authors.initials: LL
authors.lastname: Munn
mesh_terms: D056704:Adaptive Immunity; D060890:B7-H1 Antigen / Q000037:antagonists & inhibitors / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007107:Immune System / Q000378:metabolism; D007249:Inflammation; D035683:MicroRNAs / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009369:Neoplasms / Q000276:immunology / Q000473:pathology* / Q000628:therapy
chemical_list: D060890:B7-H1 Antigen; D015815:Cell Adhesion Molecules; D016207:Cytokines; D035683:MicroRNAs; D016328:NF-kappa B