c-Myc, genome instability, and tumorigenesis: the devil is in the details.
The c-myc oncogene acts as a pluripotent modulator of transcription during normal cell growth and proliferation. Deregulated c-myc activity in cancer can lead to excessive activation of its downstream pathways, and may also stimulate changes in gene expression and cellular signaling that are not observed under non-pathological conditions. Under certain conditions, aberrant c-myc activity is associated with the appearance of DNA damage-associated markers and karyotypic abnormalities. In this chapter, we discuss mechanisms by which c-myc may be directly or indirectly associated with the induction of genomic instability. The degree to which c-myc-induced genomic instability influences the initiation or progression of cancer is likely to depend on other factors, which are discussed herein.
Wade
M
M
Gene Expression Lab, The Salk Institute, 10010 N. Torrey Pines Rd., La Jolla, CA 92037, USA.
Wahl
G M
GM
D000818:Animals; D002453:Cell Cycle; D004249:DNA Damage; D004260:DNA Repair; D005786:Gene Expression Regulation; D016259:Genes, myc; D042822:Genomic Instability; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics* / Q000378:metabolism; D009857:Oncogenes; D009858:Oncogenic Viruses / Q000472:pathogenicity; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species