• Open Access

Chromosome-mediated alterations of the MYC gene in human cancer


*Correspondence to: Nicholas C. POPESCU, MD, PhD Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute,37 Convent Drive MSC 4258, Bethesda, Maryland, 20892-4258, USA. Tel: (301) 496-5688x202, Fax: (301) 496-0734. E-mail: popescun@dc37a.nci.gov


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. Protooncogenes 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.