Alternate Forms of MYB: Consequences of Virus Insertion in Myeloid Tumorigenesis and Alternative Splicing in Normal Development

Abstract

Nearly half of the proto-oncogenes were first identified in the genome of highly oncogenic avian and mammalian retroviruses (for review, see Bishop 1985). Several of these oncogenes appear to selectively transform cells of a particular lineage of differentiation. Studies on the v-myb containing avian myeloblastosis virus (AMV) and E-26 leukemia virus suggest that the viral oncogene v-myb is closely associated with myeloid tumorigenesis (for review, see Graf 1988). The transduction that gave rise to v-myb truncated the protooncogene c-myb at both of its ends. It is conceivable that myb may have multiple functions carried out by different structural domains. Removal of any of these domains may abolish either some function(s) performed by myb or its ability to be regulated by interaction with other cellular proteins. In order to understand the role of myb in normal and tumor development of myeloid cells, it is important to identify the various forms of myb in different cell types.