Journal of Environmental Pathology, Toxicology and Oncology

ISSN for PRINT: 0731-8898

For Online Access

Best Paper Award Selection - Editorial Board Site

2003, Volume22

Issue 3

92 pages

DOI: 10.1615/JEnvPathToxOncol.v22.i3

Issue price - $160.00

Sabine Mai, PhD
Manitoba Institute of Cell Biology, Cancer Care Manitoba, University of Manitoba, Winnipeg, Manitoba, Canada

J. Frederic Mushinski, MD
Molecular Genetics Section, Laboratory of Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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.

DOI: 10.1615/JEnvPathToxOncol.v22.i3.30 Download article, 21 pages

Article price - $35.00

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