Abstract
In this chapter, we will discuss the importance of genetic variations in the IL-23 receptor (IL-23R) gene in driving the process of inflammation-induced carcinogenesis. By applying bladder cancer (BLC) as a model, we will focus on two contradictory genetic mutations within the receptor gene. The first one is enhanced by cancer and induces inflammation-induced carcinogenesis via up-regulating IL-23/IL-17 inflammatory axis. However, the other preventive one deregulates this inflammatory pathway by distorting the protein nature of the receptor, leading to block its binding affinity. During the process of carcinogenesis, cancer genetically inclines the balance towards the protumor, via over-expressing the IL-23R on the surfaces of immune-bearing cells, particularly tumor-associated monocytes (TAMs) and thus increasing the levels of pro-angiogenic cytokines IL-23 and IL-17.