| First Author | Calado DP | Year | 2010 |
| Journal | Cancer Cell | Volume | 18 |
| Issue | 6 | Pages | 580-9 |
| PubMed ID | 21156282 | Mgi Jnum | J:167612 |
| Mgi Id | MGI:4868640 | Doi | 10.1016/j.ccr.2010.11.024 |
| Citation | Calado DP, et al. (2010) Constitutive canonical NF-kappaB activation cooperates with disruption of BLIMP1 in the pathogenesis of activated B cell-like diffuse large cell lymphoma. Cancer Cell 18(6):580-9 |
| abstractText | Diffuse large B cell lymphoma (DLBCL) comprises disease entities with distinct genetic profiles, including germinal center B cell (GCB)-like and activated B cell (ABC)-like DLBCLs. Major differences between these two subtypes include genetic aberrations leading to constitutive NF-kappaB activation and interference with terminal B cell differentiation through BLIMP1 inactivation, observed in ABC- but not GCB-DLBCL. Using conditional gain-of-function and/or loss-of-function mutagenesis in the mouse, we show that constitutive activation of the canonical NF-kappaB pathway cooperates with disruption of BLIMP1 in the development of a lymphoma that resembles human ABC-DLBCL. Our work suggests that both NF-kappaB signaling, as an oncogenic event, and BLIMP1, as a tumor suppressor, play causal roles in the pathogenesis of ABC-DLBCL. |
