title: Chronic inflammation and cancer: suppressing the suppressors.
abstract: Chronic inflammation typical to various chronic diseases is associated with immunosuppression, mediated primarily by immature myeloid-derived suppressor cells (MDSCs). A variety of factors induce MDSC differentiation arrest, thus manipulating the host's immune function and suppressing the innate and adaptive immune systems, as reflected by their impaired status associated with down-regulated expression of the CD247 molecule. Such chronic inflammation-induced immunosuppressive features are also found in many tumors, generating tumor micro- and macro-environments that act as critical barriers to effective anti-tumor responses and therapies. This knowledge offers new and novel candidate immune targets for therapeutic interventions, in combination with more conventional approaches as chemotherapy, radiotherapy, and cancer cell targeted therapy. Therapeutic manipulation of chronic inflammation during cancer development is likely to enhance efficacy of treatments such as vaccinations, and adoptive T cell transfer, thus switching the chronic pro-cancer inflammatory environments into an anti-cancer milieu. Based on the functional relevance of immune networking in tumors, it is advantageous to merge monitoring immune biomarkers into the traditional patient's categorization and treatment regiments, which will provide new prognostic and/or predictive tools to clinical practice. A better identification of environmental and tumor-specific inflammatory mechanisms will allow directing the clinical management of cancer toward a more personalized medicine.
authors.affiliation: Faculty of Medicine, Israel-Canada Medical Research Institute, The Lautenberg Center for General and Tumor Immunology, The Hebrew University, POB: 12272, 91120, Jerusalem, Israel, baniyash@cc.huji.ac.il.
authors.forename: Michal
authors.initials: M
authors.lastname: Baniyash
authors.forename: Moshe
authors.initials: M
authors.lastname: Sade-Feldman
authors.forename: Julia
authors.initials: J
authors.lastname: Kanterman
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000737:chemistry; D015415:Biomarkers / Q000378:metabolism; D017252:CD3 Complex / Q000378:metabolism; D006098:Granulocytes / Q000166:cytology; D006801:Humans; D007166:Immunosuppressive Agents / Q000737:chemistry; D007249:Inflammation / Q000473:pathology*; D051379:Mice; D009000:Monocytes / Q000166:cytology; D022423:Myeloid Cells / Q000166:cytology*; D009369:Neoplasms / Q000473:pathology*; D011379:Prognosis; D013601:T-Lymphocytes / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D015415:Biomarkers; D017252:CD3 Complex; C121704:CD3 antigen, zeta chain; D007166:Immunosuppressive Agents; D014409:Tumor Necrosis Factor-alpha