Structural Organization of Mouse c-myb Locus and the Mechanism of its Rearrangement in ABPL-2 Tumor Line Induced by Pristane and Abelson Murine Leukemia Virus

Abstract

Abelson murine leukemia virus (A-MuLV) is a replication-defective transforming retrovirus that arose by recombination of nondefective helper virus (M-MuLV) and cellular sequences present within the normal mouse genome. The latter sequences, termed abl, appear to code for the transforming properties of the virus (for review see Rosenberg and Baltimore, 1980). This virus induces in adult BALB/c mice a variety of lymphoid neoplasms predominantly of the pre-B cell series (ABLS tumors). However, when the mice are previously injected with pristane, which induces intraperitonal granulomatous tissue, this virus also rapidly induces plasmacytomas (ABPC tumors) and occasionally, a morphological subset of lymphosarcomas characterized by plasmacytoid cytoplasm but with very little immunoglobulin production (ABPL tumors) (Potter et al.,1978). Our preliminary experiments indicated that ABPC and ABLS tumors produced abundant amounts of infectious A-MuLV particles while most ABPL tumors, in striking contrast, did not. In an effort to understand the molecular mechanisms involved in the genesis of these tumors, a detailed study of the expression of abl, myc and myb oncogenes was undertaken (Mushinski et al., 1983).