| Literature DB >> 12381789 |
Katrina K Hoyer1, Samuel W French, Devin E Turner, Mai T N Nguyen, Mathilde Renard, Cindy S Malone, Sonja Knoetig, Chen-Feng Qi, Thomas T Su, Hilde Cheroutre, Randolph Wall, David J Rawlings, Herbert C Morse, Michael A Teitell.
Abstract
The TCL1 protooncogene is overexpressed in many mature B cell lymphomas, especially from AIDS patients. To determine whether aberrant expression promotes B cell transformation, we generated a murine model in which a TCL1 transgene was overexpressed at similar levels in both B and T cells. Strikingly, transgenic mice developed Burkitt-like lymphoma (BLL) and diffuse large B cell lymphoma (DLBCL) with attendant Bcl-6 expression and mutated J(H) gene segments at a very high penetrance beginning at 4 months of age. In contrast, only one mouse developed a T cell malignancy at 15 months, consistent with a longer latency for transformation of T cells by TCL1. Activation of premalignant splenic B cells by means of B cell antigen receptor (BCR) engagement resulted in significantly increased proliferation and augmented AKT-dependent signaling, including increased S6 ribosomal protein phosphorylation. Transgenic spleen cells also survived longer than wild-type spleen cells in long-term culture. Together these data demonstrate that TCL1 is a powerful oncogene that, when overexpressed in both B and T cells, predominantly yields mature B cell lymphomas.Entities:
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Year: 2002 PMID: 12381789 PMCID: PMC137894 DOI: 10.1073/pnas.212410199
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205