Retrovirally induced murine B-cell tumors rarely show proviral integration in sites common in T-cell tumors

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Abstract
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.