BMI-1 TRANSGENE INDUCES LYMPHOMAS AND COLLABORATES WITH MYC IN TUMORIGENESIS
- Author(s)
- Haupt, Y; Bath, ML; Harris, AW; Adams, JM;
- Details
- Publication Year 1993-11,Volume 8,Issue #11,Page 3161-3164
- Journal Title
- ONCOGENE
- Publication Type
- Journal Article
- Abstract
- The bmi-1 gene was discovered as a frequent target of Moloney virus insertion in virally accelerated B-lymphoid tumors of Emu-myc transgenic mice and hence is thought to collaborate with the myc gene in lymphomagenesis, but its oncogenic potential has not previously been tested directly. To determine whether bmi-1 overexpression can contribute to hematopoietic neoplasia in vivo, strains of transgenic mice were generated in which bmi-1 expression was directed to the lymphoid compartment by a coupled immunoglobulin heavy chain enhancer (Emu). Although the Emu-bmi-1 transgene was expressed in both B and T cells, lymphoid development was not perturbed. Nevertheless, 14% of the mice in the strain with highest expression have developed lymphoma. Unexpectedly, most tumors were of the T-cell lineage, although one case of B lymphoma was observed. Furthermore, cross breeding Emu-bmi-1 and Emu-myc mice established that the bmi-1 transgene markedly accelerated the onset of pre-B and B lymphomas. These results demonstrate directly that bmi-1 can contribute to lymphomagenesis in the T and B cell lineages and collaborate with the myc gene in tumor development.
- Publisher
- STOCKTON PRESS
- Keywords
- V-ETS; MICE; ONCOGENE; COOPERATION; EXPRESSION; LEUKEMIA; MODELS; VIRUS
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1993-11-01 12:00:00