The myc oncogene and lymphoid neoplasia: from translocations to transgenic mice.

The c-myc proto-oncogene encodes a nuclear phosphoprotein which probably plays a crucial role in growth control [4]. The protein has DNA-binding activity in vitro, but its function remains unknown. While avian retroviruses carrying the closely related vmyc sequence rapidly transform myeloid cells, the cellular myc gene has been strongly implicated in several types of lymphoid neoplasia. The fundamental mechanism releasing the oncogenic potential of c-myc is believed to be deregulation of its expression. Most chicken bursal lymphomas resulting from infection with avian leukosis virus, which does not itself bear an oncogene, carry a provirus near or within the c-myc gene [6]. About a quarter of T lymphomas with a retroviral aetiology also bear a c-myc-associated provirus [3]. Expression of the c-myc gene in these tumours is governed by the promotor and/or the enhancer in the viral long terminal repeat (LTR) [6, 13, 3]. In most plasmacytomas of the mouse and Burkitt lymphomas of man, a chromosome translocation couples the c-myc gene to the IgH constant region locus, presumably bringing c-myc under the control of factors that regulate heavy-chain expression [11, 8, 4].