DNA tumor viruses and colorectal cancer

Colorectal cancers (CRCs) are characterized by forms of genomic or epigenetic instability that generate a large number of genetic variations, some of which provide the growth and survival advantages necessary for neoplastic growth. The mechanistic basis of these fundamental processes is currently unknown. Herein, we review evidence that links the human polyomavirus JC virus mechanistically with these processes in CRC. We propose a model in which JC virus is ubiquitously present in the gastrointestinal tracts of healthy people and speculate that through a process that remains to be discovered, the virus becomes activated, expresses a potent oncogene, and triggers chromosomal instability and the methylator phenotype resulting in CRC.