Human colorectal carcinoma (CRC) is one of the leading cancers. Every year, the WHO estimates a total of 945,000 new CRC cases, with 492,000 deaths worldwide. Most CRCs arise from the main premalignant lesion, colorectal adenomas, and the progression of colorectal adenoma to CRCs may take a long-term time course. The development of human CRCs is not only determined by the adenomatous cells, but also by the interaction between adenomatous cells and host immune environment. In response to tumor initiation or invasion, many inflammatory cells and components will be inevitably activated and form an inflammatory microenvironment surrounding the CRC tumors. Accumulative evidence has revealed that inflammatory response plays a key role in the development of human CRCs by implicating in many aspects including in determining the microenvironmental immune function shift from immunosurveillance to immunosuppression and significantly influences the progression of precancerous lesions to cancers. In this review, the functional changes of immune microenvironment from precancerous stage (adenoma) to cancer stage are summarized, and their potential as predictive biomarkers and biotherapeutic significance in preventing the development of CRCs are discussed.

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It has been well documented that interleukin (IL)-17A mainly produced by the newly identified T cell subtype Th17 cells is an important proinflammatory cytokine that plays a vital pathogenic role in the process of human inflammatory bowel diseases. Recently, new information concerning the biological activities of IL-17A relating to the development of colorectal cancer (CRC) has also been reported. The present mini-review focuses on recent observations concerning the role of IL-17A in the development of CRCs, and it discusses the clinical significance of IL-17A as a biomarker and potential therapeutic target.