Loss of viral gene expression and retention of tumorigenicity by Abelson lymphoma cells.
Lymphomas induced by the Abelson murine leukemia virus (A-MuLV) were examined for the expression of biochemical and biological markers associated with A-MuLV transformation before and after in vivo growth in genetically distinguishable host mice. Although all tumors and clonal lines derived from them initially expressed the A-MuLV-encoded gag fusion protein p160, they ceased synthesis of this molecule after several weeks of growth in vivo as ascites tumors. Transplanted clonal lines continued to express the alloantigenic marker H-2b and the isoenzyme marker Gpi-1b of the donor tumor cells, indicating that the cells were of donor and not host origin. Examination of cellular DNA obtained from p160-positive and derivative p160-negative lines indicated that p160-negative clones had lost A-MuLV-specific proviral sequences as detected by hybridization with several probes. Although the clonal lines no longer expressed p160, they retained their malignant phenotype and continued to express the Abelson antigen, a cell surface marker associated with A-MuLV lymphomagenesis. Continued expression of the A-MuLV genome was not required for maintenance of oncogenic potential under these conditions of in vivo tumor growth.
D000011:Abelson murine leukemia virus / Q000235:genetics*; D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D002999:Clone Cells; D004279:DNA, Viral / Q000032:analysis; D015683:Gene Products, gag; D005814:Genes, Viral; D009052:Leukemia Virus, Murine / Q000235:genetics*; D007942:Leukemia, Experimental / Q000382:microbiology*; D008223:Lymphoma / Q000382:microbiology*; D051379:Mice; D009368:Neoplasm Transplantation; D014764:Viral Proteins / Q000096:biosynthesis*
D004279:DNA, Viral; D015683:Gene Products, gag; D014764:Viral Proteins