Obesity-Induced Chronic Low-Level Inflammation and Cancers

The World Health Organization (WHO) has highlighted “overweight and obesity” as a public health concern and a significant risk factor for several chronic diseases, including diabetes, cardiovascular diseases, and cancers. The association between the different factors that can lead to the chronic inflammatory condition in the obese persons and their effect in tumorigenesis and several cancers (esophageal, liver, colon, postmenopausal breast, and endometrial cancers) have been partially unraveled. The functional association between inflammation and cancer is not new. Existing hypotheses of obesity-associated cancer underline direct effects of dietary ingredients or metabolic imbalance in the body. The recent evidences suggest a significant connection between chronic inflammation and cancer risk, possibly involving dietary and metabolic components. In the nineteenth century, Virchow first addressed the involvement of immune cells in tumorigenesis (Balkwill and Mantovani, The Lancet 357:539–545, 2001). The mediators and cellular effectors of inflammation are essential components of the tumor microenvironment and are more likely to contribute to tumor growth, its development and immunosuppression (Coussens and Werb, Nature 420:860–867, 2002). A strong relationship of chronic inflammation with malignant diseases can be traced in several individuals with inflammatory bowel diseases, such as Ulcerative colitis and Crohn’s disease, also developing colon carcinogenesis. Further, hepatitis C infection in the hepatic cells has been predisposed to liver carcinoma. Understanding these molecular pathways of cancer-related inflammation could lead to identification of new target molecules for improved diagnosis and treatment regimes. In this chapter, we will critically discuss the roles of cytokines, chemokines, growth factors, and inflammatory signaling pathways related to obesity and cancer risk.