Avian v-myc replaces chromosomal translocation in murine plasmacytomagenesis.
Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.
D000818:Animals; D001717:Birds; D002471:Cell Transformation, Neoplastic; D005814:Genes, Viral; D051379:Mice; D008807:Mice, Inbred BALB C; D008815:Mice, Inbred Strains; D008979:Moloney murine leukemia virus / Q000235:genetics*; D009693:Nucleic Acid Hybridization; D009857:Oncogenes; D010954:Plasmacytoma / Q000235:genetics / Q000382:microbiology*; D012190:Retroviridae / Q000235:genetics*; D014158:Transcription, Genetic; D014178:Translocation, Genetic