Mario Gomez

TL;DR: It is found that clinical isolates of several types of B cell lymphomas, including diffuse large B Cell lymphoma (DLBCL), have 10- to 30-fold higher copy numbers of miR-155 than do normal circulating B cells, and the quantities of BIC RNA are elevated in lymphoma cells, but ratios of the amounts of the two RNAs are not constant, suggesting that the level of mi R-155 is controlled by transcription and processing.

TL;DR: This study identifies PRDM1 inactivation as a recurrent genetic defect in DLBCL cells and establishesPRDM1 as a potential tumor suppressor gene inDLBCL, and demonstrates for the first time the potential role of RNA editing in lymphomagenesis.

TL;DR: MiRNA-mediated down-regulation of PRDM1/Blimp-1 may contribute to the phenotype maintenance and pathogenesis of HRS cells by interfering with normal B-cell terminal differentiation, thus representing a novel molecular lesion, as well as a potential therapeutic target in HL.

TL;DR: This study demonstrates for the first time clonal transformation of CLL/SLL into IDCS, a rare tumor derived from interdigitating dendritic cells, triggered by alterations in lineage-determining transcription programs, which result in transdifferentiation, coupled with additional oncogenic stimuli caused by chromosomal imbalances.

TL;DR: Data obtained from expression analysis, luciferase reporter assays, and transfection experiments support a role of targeting of PRDM1 by microRNA let-7 family in mediating this down-regulation and provide further evidence for an important role of impairment of terminal B cell differentiation in DLBCL pathogenesis.