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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.625 5-Year IF: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvPathToxOncol.v22.i3.30
21 pages

c-Myc-Induced Genomic Instability

Sabine Mai
Manitoba Institute of Cell Biology, Cancer Care Manitoba, University of Manitoba, Winnipeg, Manitoba, Canada
J. Frederic Mushinski
Molecular Genetics Section, Laboratory of Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

ABSTRACT

c-myc is one of a small family of proto-oncogenes that do not require mutation to contribute to neoplastic transformation. Instead, the deregulated expression of the oncoprotein at even modest levels is sufficient to initiate this process. The transforming activity of c-Myc is generally thought to lie in its ability to modulate the expression of a series of genes, among them certain proliferation-promoting genes. In reality, c-Myc is a multifunctional protein that also affects the stability of the genome. In this review, we summarize the growing evidence that deregulated c-myc expression generates genomic instability by initiating gene amplification (both intra- and extra-chromosomally), gene rearrangements, and karyotypic instability. Cancer is a disease of impaired genomic stability, to which c-Myc contributes during its initiation and progression through the induction of genomic instability in critical genes. Myc thus acts as a structural modifier of the genome and as a promoter of neoplastic transformation.


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