Interleukin-1 (IL-1) and the inflammasome in cancer. (May 2022)

• Record Type: Journal Article
• Authors: Pretre, Vincent; Papadopoulos, Dimitrios; Regard, Jean; Pelletier, Marc; Woo, Janghee
• Is Part Of: Cytokine. Volume 153(2022)
• Publication Date: 2022-05
• Subjects: IL-1β -- NLRP3 -- Inflammasome -- Cancer -- Tumor microenvironment -- Tumor-promoting inflammation; ADCC antibody-dependent cellular cytotoxicity -- AIM2 absent in melanoma 2 -- ALL acute lymphoblastic leukemia -- AOM azoxymethane -- ASC apoptosis-associated speck-like protein containing a caspase activation and recruitment domain -- ASCO American Society of Clinical Oncology -- Bcl-2 B-cell lymphoma 2 -- CANTOS Canakinumab Anti-inflammatory Thrombosis Outcome Study -- CAPS cryopyrin-associated periodic syndrome -- CAR chimeric antigen receptor -- CARD caspase activation and recruitment domain -- CAR-T chimeric antigen receptor T-cell -- CD cluster of differentiation -- CI confidence interval -- CMML chronic myelomonocytic leukemia -- CRS cytokine-release syndrome -- CtDNA circulating tumor DNA -- DAMP damage-associated molecular pattern -- DC dendritic cell -- DLT dose-limiting toxicity -- DNA deoxyribonucleic acid -- DSS dextran sulfate sodium -- EAE experimental autoimmune encephalomyelitis -- ESA erythrocyte stimulating agent -- FDA food and drugs administration -- FMF Familial Mediterranean Fever -- HNSCC head and neck squamous cell carcinoma -- hs-CRP high-sensitivity C-reactive protein -- ICANS immune effector cell-associated neurotoxicity syndrome -- IFN-γ interferon-γ -- IL-1 interleukin 1 -- IL-1R IL-1 receptor -- IL-1Ra IL-1R antagonist -- IL-1RAP interleukin 1 receptor accessory protein -- IL-6 interleukin 6 -- IL-18 interleukin 18 -- IL-18BP IL-18 binding protein -- IPSS International Prognostic Scoring System -- IV intravenous -- MAPK mitogen activated protein kinase -- MDS myelodysplastic syndrome -- MDSC myeloid-derived suppressor cell -- MM multiple myeloma -- NF-κB nuclear factor kappa light chain enhancer of activated B cells -- NHL Non-Hodgkin's lymphoma -- NK natural killer -- NLR nucleotide-binding domain and leucine-rich repeat receptor -- NLRC NLR family CARD containing -- NLRP NLR family pyrin domain containing -- NSCLC non-small cell lung cancer -- OS overall survival -- PAMP pathogen-associated molecular pattern -- PD-1 programmed cell death protein 1 -- PD-L1 programmed death ligand 1 -- PDAC pancreatic ductal adenocarcinoma -- PFS progression free survival -- PRR pattern recognition receptor -- q3w every 3 weeks -- q8w every 8 weeks -- RIG-I retinoic acid-inducible gene I -- S1P sphingosine-1-phosphate -- SC subcutaneous -- TAM tumor-associated macrophage -- Th T helper -- TIM-3 T cell immunoglobulin and mucin-containing molecule 3 -- TMEM176B transmembrane protein 176B -- VEGF vascular endothelial growth factor -- VEGFR vascular endothelial growth factor receptor; Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2022.155850
• Languages: English
• ISSNs: 1043-4666

Abstract

Highlights: Inflammasomes and the IL-1 cytokine family can promote tumorigenesis. Inflammasomes are involved in multiple cellular interactions beyond innate immunity. Inhibition of IL-1β lowers incidence and mortality of lung cancer. IL-1/inflammasome pathways are being targeted in multiple clinical investigations. Anti-cytokine/inflammasome therapy might be more effective in earlier stages of disease. Abstract: Numerous preclinical and clinical studies have demonstrated the significant contribution of inflammation to the development and progression of various types of cancer. Inflammation in the tumor microenvironment mediates complex interactions between innate immunity, adaptive immunity, microbiomes and stroma, and ultimately alters the overall fitness of tumor cells at multiple stages of carcinogenesis. Malignancies are known to arise in areas of chronic inflammation and inflammation in the tumor microenvironment (often called tumor-promoting inflammation) is believed to allow cancer cells to evade immunosurveillance while promoting genetic instability, survival and progression. Among the strongest data suggesting a causal role for inflammation in cancer come from the recent CANTOS trial which demonstrated that interleukin-1β (IL-1β) inhibition with canakinumab leads to a significant, dose-dependent decrease in incident lung cancer. This observation has launched a series of additional clinical studies to understand the role of IL-1β and the inflammasome in cancer, and the clinical utility of IL-1β inhibition in different stages of lung cancer. In this article we will review recent data implicating IL-1β signaling and its upstream regulator NLRP3 in both solid tumor and hematologic malignancies. We will discuss the key preclinical observations and the current clinical landscape, and describe the pharmacologic tools which will be used to evaluate the effects of blocking tumor-promoting inflammation clinically.