C-myc misregulation triggers complex process of genomic instability

Genetic stability is an essential factor for the cellular integrity. Failure in its maintenance leads to accumulation of errors derived from the process of DNA replication, cellular metabolism, action of endogenous and exogenous DNA damaging factors and eventually, as a final outcome tumor initiation and progression occur. Overall manifestation of c-Myc deregulation in many tumors and different mechanisms of Myc's action toward genomic stability suggest that this gene plays a central role in destabilization of genome. Microarray studies and functional genomics approach led us to conclusion that c-Myc can control nuclear architecture in global fashion since about 15% of all cellular genes are regulated by this transcription factor. Deregulation of c-illyc gene triggers a composite network of genomic instability that may result in several different outcomes as: locus-specific amplification, formation of extrachromosomal elements (EEs), chromosomal instability, long-range illegitimate recombination, point mutations, DNA breakage and nuclear structure reorganization This review outlines the growing evidence that c-Myc oncogene induces a complex network of genomic instability and describes systems and circumstances under which deregulation of c-Myc results in specific types of genomic alteration