ABSTRACT
The myc family of nuclear proto-oncogenes have emerged as genetic elements which are likely to play a significant role in the regulation of normal mammalian development and malignant transformation. The first cellular myc gene was discovered over a decade ago by Sheiness and Bishop who demonstrated the existence of a cellular homologue of an avian myelocytomatosis virus oncogene, designated c-myc. A causal role for myc family oncogenes in malignancy is supported by their frequent deregulated expression in a variety of naturally-occurring tumors. Deregulation may be mediated by a number of mechanisms such as gene amplification, translocation, retroviral insertion, or mutation. A strong correlation exists between myc gene copy number, level of myc gene expression, and the clinical behavior of tumors. Transcriptional mechanisms controlling c-, N-, and L-myc expression were studied in small-cell lung carcinoma cell lines in which deregulation of a specific myc family gene had taken place.
