A Sgambato1, A Cittadini. 1. "Giovanni XXIII" Cancer Research Center, Institute of General Pathology, Catholic University of the Sacred Hearth, Rome, Italy. asgambato@rm.unicatt.it
Abstract
STATE OF THE ART: Mounting evidence indicates a link between inflammation and cancer. However, the molecular mechanism(s) remains unclear. Indeed, although preclinical and clinical studies suggest that chronic inflammation can promote cancer development, the role(s) of inflammation in the process is likely very complex and far to be completely understood. Inflammation can promote all stages of tumor development through multiple mechanisms which include enhanced proliferation and resistance to apoptosis of initiated cells, induction of DNA mutations, promotion of angiogenesis, invasion and metastasis. On the other hand, components of tumor microenviroment, including tumor cells themselves, may promote an inflammatory state by producing inflammatory mediators. Moreover, while chronic inflammation might promote tumor formation, acute inflammation might well hamper the process and is indeed used therapeutically to inhibit tumor formation. CONCLUSIONS: The present review briefly highlights the relationship between inflammation and tumorigenesis and discusses the possibility to develop chemoprevention and/or therapeutical approaches targeting components of the inflammatory responses.
STATE OF THE ART: Mounting evidence indicates a link between inflammation and cancer. However, the molecular mechanism(s) remains unclear. Indeed, although preclinical and clinical studies suggest that chronic inflammation can promote cancer development, the role(s) of inflammation in the process is likely very complex and far to be completely understood. Inflammation can promote all stages of tumor development through multiple mechanisms which include enhanced proliferation and resistance to apoptosis of initiated cells, induction of DNA mutations, promotion of angiogenesis, invasion and metastasis. On the other hand, components of tumor microenviroment, including tumor cells themselves, may promote an inflammatory state by producing inflammatory mediators. Moreover, while chronic inflammation might promote tumor formation, acute inflammation might well hamper the process and is indeed used therapeutically to inhibit tumor formation. CONCLUSIONS: The present review briefly highlights the relationship between inflammation and tumorigenesis and discusses the possibility to develop chemoprevention and/or therapeutical approaches targeting components of the inflammatory responses.
Authors: Haris G Vikis; Andrew E Gelman; Andrew Franklin; Lauren Stein; Amy Rymaszewski; Jihong Zhu; Pengyuan Liu; Jay W Tichelaar; Alexander S Krupnick; Ming You Journal: Mol Carcinog Date: 2011-10-17 Impact factor: 4.784
Authors: F Bussu; C Graziani; R Gallus; A Cittadini; J Galli; E DE Corso; G DI Cintio; M Corbi; G Almadori; A Boninsegna; G Paludetti; A Sgambato Journal: Acta Otorhinolaryngol Ital Date: 2018-04 Impact factor: 2.124