Chronic inflammatory diseases of the intestinal tract have been known to increase risk of developing a form of colorectal cancer known as inflammation-associated cancer. The roles of inflammation in tumor formation and development in Apc^Min/+ mice have been broadly corroborated. The Apc^Min/+ mouse model contains a point mutation in the adenomatous polyposis coli (Apc) gene and only develops intestinal precancerous lesions, the benign adenomas. Thus, it provides an excellent in vivo system to investigate the molecular events involved in the inflammatory process which may contribute to multistep tumorigenesis and carcinogenesis. Recent investigations that employ this model studied the effects of gene alterations, intestinal microorganisms, drugs, diet, exercise and sleep on the inflammatory process and tumor development, and revealed the mechanisms involved in the formation, promotion and carcinogenesis of adenomas with the background of inflammation. Herein, we focus our review on the application of the Apc^Min/+ mouse model for studying inflammation-associated intestinal tumor and find that anti-inflammation is a possible strategy in combating intestinal tumor, but sometimes anti-inflammation cannot help reduce tumor burden. Moreover, various inflammation-related genes are involved in different mechanistic stages of tumor in Apc^Min/+ mice and intricate regulatory effects of inflammation exist in the whole progression of intestinal tumor.