Retrovirally induced murine B-cell tumors rarely show proviral integration in sites common in T-cell tumors.
The molecular etiology of retrovirally induced T-cell tumors has been shown in many cases to involve proviral integration near a cellular oncogene, c-myc, N-myc, Pim-1 and pvt-1 being frequent targets for insertional activation. Murine B-cell tumors induced by infection with murine leukemia virus have been studied for rearrangements in these and other loci. In contrast to the T-cell lymphomas, tumors of the B-cell lineage, either early B-cell tumors induced in nude mice or late B-cell tumors in immunocompetent mice, did not show disruption of N-myc or Pim-1 in any of the tumors studied, although those lymphomas had acquired many new proviruses. The loci c-abl, bcl-2, fis-1, c-erbB, c-myb, and neu were likewise not involved. Rearrangement of c-myc was seen in 1 out of 71 and rearrangement of the pvt-1 locus in 4 out of 73 (5%) of the B-cell tumors. Thus it appears that mechanistic differences exist in the development of T-cell tumors and B-cell tumors caused by the same etiological agent.
Matthews
E A
EA
Division of Immunology, The Netherlands Cancer Institute, Antoni van Leeuwenhoek Huis, Amsterdam.
Vasmel
W L
WL
Schoenmakers
H J
HJ
Melief
C J
CJ
D000818:Animals; D000831:Animals, Newborn; D001402:B-Lymphocytes; D015139:Blotting, Southern; D015342:DNA Probes; D004279:DNA, Viral / Q000235:genetics; D009052:Leukemia Virus, Murine / Q000235:genetics*; D008223:Lymphoma / Q000209:etiology* / Q000235:genetics; D051379:Mice; D008815:Mice, Inbred Strains; D009693:Nucleic Acid Hybridization; D009857:Oncogenes; D011533:Proviruses / Q000235:genetics*; D013601:T-Lymphocytes
D015342:DNA Probes; D004279:DNA, Viral