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.