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

✍ Scribed by E. A. Matthews; W. L. E. Vasmel; H. J. Schoenmakers; C. J. M. Melief

• Book ID: 102868620
• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: French
• Weight: 842 KB
• Volume: 43
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910430627

✦ Synopsis

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, P i m I and pvt-I 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 P i m I in any of the tumors studied, although those lymphomas had acquired many new proviruses. The loci c-abl, bcC2, fis-I, c-erbB, c-myb, and neu were likewise not involved. Rearrangement of c-myc was seen in I out of 71 and rearrangement of the pvt-l 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.

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