c-myc Transcription is Initiated from Po in 70% of Patients with Multiple Myeloma

Abstract

The role of the c-myc gene is well established in Burkitt’s lymphoma and in murine plasmacytomas [1]. In these neoplasms the c-myc locus is involved in a reciprocal chromosomal translocation with the immunoglobulin heavy chain or light chain loci, resulting in inappropriate activation of c-myc transcription. In patients with multiple myeloma, however, the role of the c-myc gene is less clear. Less than 1% of patients with multiple myeloma have abnormalities of chromosome 8, and t(8:14) are rare [2]. At the structural level, abnormalities are seen in less than 5% of patients [2]. However, approximately 85–90% of patients show levels of c-myc mRNA and protein, in tumor cells, that are comparable to actively proliferating cells, suggesting a possible role for c-myc in this neoplasm [3]. A number of oncogenes have been shown to be abnormal in multiple myeloma [4]. Some of these genes (eg. ras) act at a proximal level in the signal transduction apparatus, while others subserve regulatory functions (eg. p53, Rb). Thus, although c-myc may be structurally normal in myeloma, its transcription may be inappropriately activated or regulated by mutations in other genes.