Mechanisms that affect the transcription of the c-myc oncogene take part in the development of B-cell neoplasias such as Burkitt's lymphoma. Daudi Burkitt lymphoma cells, which express only the translocated c-myc oncogene, were hybridized with human lymphoblastoid cells, which express the normal c-myc gene; the hybrids were phenotypically lymphoblastoid and expressed both the translocated and the normal c-myc gene. This result contrasts with the findings that the decapitated c-myc gene, translocated to an immunoglobulin switch mu or alpha region, is transcriptionally silent in lymphoblastoid hybrids. Thus, there may be at least two distinct enhancer-like elements capable of deregulating c-myc transcription in lymphomas and leukemias with t(8;14) chromosome translocations. In addition, since the Daudi X lymphoblastoid hybrids express both the translocated and the normal c-myc gene, the c-myc gene product does not autoregulate c-myc transcription.