Adina Grunn

TL;DR: The results demonstrate that NF-κB activation in DLBCL is caused by genetic lesions affecting multiple genes, the loss or activation of which may promote lymphomagenesis by leading to abnormally prolonged NF-σκB responses.

TL;DR: By combining next-generation sequencing and copy number analysis, it is shown that the DLBCL coding genome contains, on average, more than 30 clonally represented gene alterations per case and novel dysregulated pathways underlying its pathogenesis are identified.

TL;DR: The results identify CREBBP/EP300 mutations as a major pathogenetic mechanism shared by common forms of B-cell non-Hodgkin’s lymphoma, with direct implications for the use of drugs targeting acetylation/deacetylation mechanisms.

TL;DR: Next generation sequencing and copy number analysis provide insights into the complexity of the CLL coding genome, and reveal an association between NOTCH1 mutational activation and poor prognosis.

TL;DR: Findings point to a role for BLIMP1 as a tumor suppressor gene, whose inactivation may contribute to lymphomagenesis by blocking post–GC differentiation of B cells toward plasma cells, and suggest that the same gene is inactivated by epigenetic mechanisms in an additional large number of cases.