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The human colorectal tumorigenesis model proposed by Vogelstein and colleagues [12,13] describes sequential inactivation of tumor suppressors (APC, SMAD4, and P53), activation of oncogene KRAS, and development of genomic instability. However, genes that are near the bona fide tumor suppressors and are disrupted in the human CRC appear not to be cancer-drivers, based on mouse model studies (DCC) or due to lack of evidence for the contribution to cancer (MCC).
