Mutations of tumor suppressor genes, of the mismatch DNA repair system, and of the TGF-beta-II-receptor are the main causes for a higher risk of colorectal cancer. Among mutations of the Ape gene, which characterize the clinical manifestation of the familial polyposis (FAP), point mutations are dominating which create new stop codons or arise from deletions or insertions of nucleotides causing frame shifts. Because the binding site of beta-catenin is localized in the C-terminus of the Ape protein, disturbances result in the cellular signal transfer from its loss. Consequently, the interactions of the usually formed Ape-beta-catenin complex with the cytoskeleton and the cadherin system in the plasma membrane as well as the translocation of beta-catenin into the nucleus cannot be realized. Mutations in the genes of the mismatch DNA repair system and of the TGF-beta-II-receptor, the main defects of the HNPCC (hereditary nonpolyposis colorectal cancer), are exclusively identified in sequences of microsatellites. Because the majority of Apc gene mutations is also localized in repetitive motifs even in CpG islands primary disturbances are to postulate in the methylation pattern of the genes producing germline and somatic mutations. Generally, complexly connected reactions are involved in this cascade of colorectal cancer genesis. This fact explains the relatively late clinical manifestation of the disease and offers the possibility to identify carriers with an increased risk of colorectal cancer development in order to integrate them into a programme of control and preventive medicine. Beside the known treatment by surgery and cytostatics, inhibitors of prostaglandin synthesis gain therapeutic significance. Cancerogenesis can be efficiently suppressed by inhibition of the COX-2-induction (cyclo-oxygenase-2). There is a lack of clinical experience for a decision whether a high intraluminal level of butyrate in the large intestine can delay colorectal carcinogenesis.