Deregulated c-myc expression in Epstein-Barr-virus-immortalized B-cells induces altered growth properties and surface phenotype but not tumorigenicity.

Endemic Burkitt's lymphoma (eBL) is characterized by the presence of Epstein-Barr virus (EBV) and a chromosomal translocation which results in deregulation and constitutive expression of the c-myc proto-oncogene. In order to examine the role played by activation of c-myc in determining the eBL phenotype, we have introduced into EBV-immortalized lymphoblastoid cells (LCL) plasmids which permit constitutive expression of c-myc. The resulting cells show a reduced serum dependence, reduced homotypic cell aggregation, and changes in surface characteristics. In particular, levels of the cell adhesion molecule, LFA-I, are greatly reduced. However, the cells continue to express all the EBV latent antigens associated with the LCL phenotype and they remain nontumorigenic. These results suggest that, whilst constitutive expression of c-myc may contribute to the malignant phenotype, it is insufficient to induce tumorigenicity.