Chromosome-mediated alterations of the MYC gene in human cancer.
The step-wise accumulation of genetic and epigenetic alterations in cancer development includes chromosome rearrangements and viral integration-mediated genetic alterations that frequently involve proto-oncogenes. Proto-oncogenes deregulation lead to unlimited, self-sufficient cell growth and ultimately generates invasive and destructive tumors. C-MYC gene, the cellular homologue of the avian myelocitic leukemia virus, is implicated in a large number of human solid tumors, leukemias and lymphomas as well as in a variety of animal neoplasias. Deregulated MYC expression is a common denominator in cancer. Chromosomal rearrangements and integration of oncogenic viruses frequently target MYC locus, causing structural or functional alterations of the gene. In this article, we illustrate how genomic rearrangements and viruses integration affect MYC locus in certain human lymphomas and solid tumors.
Popescu
N C
NC
Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, 37 Convent Drive MSC 4258, Bethesda, Maryland 20892-4258, USA. popescun@dc37a.nci.nih.gov
Zimonjic
D B
DB
D001943:Breast Neoplasms / Q000235:genetics; D002051:Burkitt Lymphoma / Q000235:genetics; D002869:Chromosome Aberrations; D005784:Gene Amplification; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics / Q000821:virology; D009369:Neoplasms / Q000235:genetics*; D009857:Oncogenes; D009858:Oncogenic Viruses / Q000235:genetics; D011995:Recombination, Genetic; D014178:Translocation, Genetic; D014407:Tumor Cells, Cultured; D016662:Virus Integration