Suppression of the malignant phenotype in somatic cell hybrids between Burkitt's lymphoma cells and Epstein-Barr virus-immortalized lymphoblastoid cells despite deregulated c-myc expression.

To approach the question whether the absence of specific cellular gene functions may be involved in Burkitt's lymphoma pathogenesis, somatic cell hybrids were established between a malignant Epstein-Barr virus (EBV) positive Burkitt's lymphoma cell line (BL 60) and a nonmalignant EBV-immortalized lymphoblastoid cell line (IARC 277) derived from the same individual. The hybrids revealed a near tetraploid karyotype including one copy of the 8q+ chromosome resulting from the Burkitt's lymphoma-specific translocation t(8;22) in addition to three apparently normal copies of chromosome 8. Although the hybrid cells exhibited the deregulated c-myc expression pattern of the parental Burkitt's lymphoma cell line with highly abundant transcripts originating from the 8q+ chromosome, their growth characteristics in tissue culture as well as in nude mice were identical to that of the parental nonmalignant lymphoblastoid cell line. These data indicate that, at least in the system described here, the malignant phenotype of Burkitt's lymphoma cells can be suppressed by introduction of an additional set of apparently normal chromosomes from the same individual and that EBV infection and c-myc deregulation may not be sufficient for maintenance of the malignant phenotype.