Retrovirally induced murine B-cell tumors rarely show proviral integration in sites common in T-cell tumors
| Autor: | H. J. Schoenmakers, Cornelis J. M. Melief, W. L. E. Vasmel, E. A. Matthews |
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| Rok vydání: | 1989 |
| Předmět: |
Cancer Research
Lymphoma T-Lymphocytes T cell Mice Inbred Strains Biology Virus Mice Proviruses hemic and lymphatic diseases Murine leukemia virus medicine Animals B cell B-Lymphocytes Oncogene Nucleic Acid Hybridization Oncogenes Gene rearrangement Provirus medicine.disease biology.organism_classification Virology Leukemia Virus Murine Blotting Southern medicine.anatomical_structure Animals Newborn Oncology DNA Viral Cancer research DNA Probes |
| Zdroj: | International Journal of Cancer. 43:1120-1125 |
| ISSN: | 1097-0215 0020-7136 |
| DOI: | 10.1002/ijc.2910430627 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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