Abstract
SUMMARY Somatic mutations in key driver genes are necessary for colorectal tumor formation. Whereas the majority of sporadic colorectal cancer (CRC) cases have chromosomal instability, a sixth of cases generate somatic mutations by a deficiency in the mismatch repair system. This choice of mutational mechanism has a strong impact on which genes in CRC pathways are the most likely to be mutated in an individual tumor. A specific challenge in understanding CRC with microsatellite instability is to discriminate driver from passenger genes given the large number of nucleotide repeats that are frequently found mutated in patient tumors. This review, therefore, discusses strategies for the identification and validation of cancer genes in microsatellite-unstable colorectal cancers.
Published Version
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