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A review of canakinumab and its therapeutic potential for non-small cell lung cancer

Schenk, Kara M.a; Reuss, Joshua E.a; Choquette, Karinb,,c; Spira, Alexander I.a,,b,,c

doi: 10.1097/CAD.0000000000000832
Review Article
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Inflammation is essential for our innate and adaptive immunity, but chronic inflammation can also be detrimental, playing a role in tumor development and subversion of host immunity. A multitude of proteins and cytokines are involved in chronic inflammation; interleukin-1β, in particular, has been recognized as a critical pro-inflammatory cytokine that can trigger a cascade of inflammatory mediators, promoting angiogenesis, tumor invasiveness, and metastasis. The inhibition of interleukin-1β with the antibody canakinumab was recently highlighted in a large-scale trial studying the effects of the inflammatory modulating antibody in heart disease. In this study, a marked decrease in the incidence of lung cancer (a 67% relative risk reduction) was observed in a high-risk population. Although a number of preclinical studies have demonstrated that canakinumab inhibits interleukin-1β and reduces inflammation, the question remains whether these actions positively affect both cancer incidence and recurrence. This review will summarize the role of inflammation in cancer propagation and development, discuss the biological rationale for targeting interleukin-1β in lung cancer, advocate for further investigation of the anti-inflammatory antibody canakinumab as a new attractive mechanism for future lung cancer therapy, and discuss future and ongoing trials.

aJohns Hopkins School of Medicine, Baltimore, Maryland

bVirginia Cancer Specialists (VCS), Fairfax, Virginia

cUS Oncology Research, The Woodlands, Texas, USA

Received 22 April 2019 Revised form accepted 22 July 2019

Correspondence to Alexander I. Spira, Virginia Cancer Specialists, 8503 Arlington Blvd Suite 400, Fairfax, VA 22031, USA, Tel: +1 703 280 5390; fax: +1 703 280 9596; e-mail:Alexander.spira@usoncology.com

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