Inflammatory Biomarkers and Risk of Lung Cancer

Extract

About a century ago, the visionary cell biologist Theodor Heinrich Boveri postulated that tumorigenesis is promoted by chronic inflammation and that “parasites” can promote tumorigenesis by inducing inflammation ( 1 ). Several infectious agents have now been documented to cause cancer in humans. Whereas specific molecular processes are implicated as key players in cancer pathogenesis from hepatitis B virus and certain types of human papillomavirus infections, chronic inflammation is likely to play a key role in the development of hepatocellular carcinoma from hepatitis C virus infection ( 2 , 3 ). Moreover, several investigations including prospective cohort studies on the association of C-reactive protein (CRP), a nonspecific systematic marker of chronic inflammation, with cancer occurrence indicated that individuals with elevated levels of serum CRP are at increased risk for a spectrum of cancer types that do not have a predominant infectious etiology, including lung cancer ( 4–6 ). It appears that chronic inflammation, whether induced by biological agents or other exposures such as smoking ( 7 ), has reentered a center stage as a pathogenic process in cancer causation. A recent review article ( 8 ) summarized that inflammation may be involved in several stages of carcinogenesis, from tumor initiation to tumor promotion and even metastatic progression, through mechanisms involving genomic instability, epigenetic modifications, localized immunosuppression, and angiogenesis. With respect to lung cancer, clinical studies have suggested that high serum levels of interleukin 6 (IL-6) and interleukin 8 (IL-8) are associated with increased risk of the disease ( 9 , 10 ).