Author/Authors :
Giorgio Cattoretti، نويسنده , , Giorgio and Pasqualucci، نويسنده , , Laura and Ballon، نويسنده , , Gianna and Tam، نويسنده , , Wayne and Nandula، نويسنده , , Subhadra V. and Shen، نويسنده , , Qiong and Mo، نويسنده , , Tongwei and Murty، نويسنده , , Vundavalli V. and Dalla-Favera، نويسنده , , Riccardo، نويسنده ,
Abstract :
Summary
e large B cell lymphomas (DLBCL) derive from germinal center (GC) B cells and display chromosomal alterations deregulating the expression of BCL6, a transcriptional repressor required for GC formation. To investigate the role of BCL6 in DLBCL pathogenesis, we have engineered mice that express BCL6 constitutively in B cells by mimicking a chromosomal translocation found in human DLBCL. These mice display increased GC formation and perturbed post-GC differentiation characterized by a decreased number of post-isotype switch plasma cells. Subsequently, these mice develop a lymphoproliferative syndrome that culminates with the development of lymphomas displaying features typical of human DLBCL. These results define the oncogenic role of BCL6 in the pathogenesis of DLBCL and provide a faithful mouse model of this common disease.
