ABSTRACT
It is well known that chronic inˆammation is closely related to several malignancies. Once cells are activated by inˆammatory stimuli, both reactive oxygen/nitrogen species (ROS/RNS) are massively generated, which cause irreversible DNA damage (Kundu and Surh 2008). Thus, chronic inˆammation itself can act as an initiator of the multistage carcinogenesis. Furthermore, proinˆammatory cytokines and chemokines released from the inˆamed cells can overactivate various cellular signaling molecules, such as nuclear factor κB (NF-κB) and hypoxia-inducible factor-1 α (HIF-1α), leading to promotion and progression of cancer as well as profound inˆammation (Cramer and Johnson 2003; Cramer et al. 2003; Frede et al. 2005; Karin and Greten 2005). This vicious cycle of chronic inˆammation might accelerate carcinogenesis.
