The differentiation of B-cells, unlike other hematopoietic cells that develop in a single burst, occurs in interrupted steps. As a consequence there are different types of B-cells that are distinguished by their level of development. Accordingly there are a variety of different kinds of B-cell tumors. The most common proto-oncogene that is mutated in B-cell tumors is c-myc. In mammalian systems c-myc is mutated by chromosomal rearrangements with immunoglobulin-gene-bearing chromosomes. The c-myc gene may be directly rearranged in some translocations but in a number of others the breaksites are only near the c-myc locus. The mechanism of dysregulation of myc transcription in the latter is currently being investigated. Probably the most striking finding is the number of different B-cell tumor-forming systems in different species in which one or more of the characteristic 'myc' chromosomal translocations occur. In humans these occur in eBL, sBL and AIDS-associated lymphomas. B-cell lymphomas. Dysregulation of c-myc is a major phenotype in many (but not all) B-cell tumors and further does not appear to be sufficient to establish an autonomously growing B-cell. Surprisingly the nature of the additional changes has not been determined in B-cell tumor systems. It is known though that when certain other oncogenes are passively introduced into cells with dysregulated c-myc genes autonomously growing phenotypes do emerge. The oncogenes known to cooperate with a dysregulated myc (e.g. Ha-ras, raf-1 and v-abl) are thought to code for proteins that participate in growth-factor-induced signal transductions.