| First Author | Linette GP | Year | 1995 |
| Journal | Blood | Volume | 86 |
| Issue | 4 | Pages | 1255-60 |
| PubMed ID | 7632929 | Mgi Jnum | J:28635 |
| Mgi Id | MGI:76156 | Doi | 10.1182/blood.v86.4.1255.bloodjournal8641255 |
| Citation | Linette GP, et al. (1995) Peripheral T-cell lymphoma in lckpr-bcl-2 transgenic mice. Blood 86(4):1255-60 |
| abstractText | t(14;18) is the most common translocation in human lymphoid malignancy and results in bcl-2 overexpression. Bcl-2 blocks apoptosis and constitutes the initial member of a new category of oncogenes, ie, regulators of cell death. Bcl-2-Ig transgenic mice develop follicular hyperplasia and progress to malignant B-cell lymphoma. To assess the oncogenic potential of bcl-2 in the T-cell lineage, a cohort of 68 lckpr-bcl-2 transgenic mice and 56 control littermates were monitored for signs of malignancy over a 24-month period. Eighteen (26%) lckpr-bcl-2 mice developed diffuse, predominantly large-cell lymphomas at a mean age of 18 months. In contrast, only one nontransgenic control mouse developed lymphoma. CD3 surface expression and clonal T-cell receptor beta rearrangements support the T-lineage classification of these neoplasms. lckpr-bcl-2-enforced lymphomas are predominantly CD4+CD8-, consistent with a mature peripheral T-cell phenotype. These data provide support for the thesis that violation of homeostasis through the repression of cell death can be a primary mechanism of tumorigenesis in multiple lineages. |
