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- W2129650489 abstract "Richter syndrome (RS) derives from the rare transformation of chronic lymphocytic leukemia (CLL) into an aggressive lymphoma, most commonly of the diffuse large B cell lymphoma (DLBCL) type. The molecular pathogenesis of RS is only partially understood. By combining whole-exome sequencing and copy-number analysis of 9 CLL-RS pairs and of an extended panel of 43 RS cases, we show that this aggressive disease typically arises from the predominant CLL clone by acquiring an average of ∼20 genetic lesions/case. RS lesions are heterogeneous in terms of load and spectrum among patients, and include those involved in CLL progression and chemorefractoriness (TP53 disruption and NOTCH1 activation) as well as some not previously implicated in CLL or RS pathogenesis. In particular, disruption of the CDKN2A/B cell cycle regulator is associated with ∼30% of RS cases. Finally, we report that the genomic landscape of RS is significantly different from that of de novo DLBCL, suggesting that they represent distinct disease entities. These results provide insights into RS pathogenesis, and identify dysregulated pathways of potential diagnostic and therapeutic relevance." @default.
- W2129650489 created "2016-06-24" @default.
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- W2129650489 date "2013-10-14" @default.
- W2129650489 modified "2023-10-16" @default.
- W2129650489 title "Genetic lesions associated with chronic lymphocytic leukemia transformation to Richter syndrome" @default.
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- W2129650489 doi "https://doi.org/10.1084/jem.20131448" @default.
- W2129650489 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3804949" @default.
- W2129650489 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24127483" @default.
- W2129650489 hasPublicationYear "2013" @default.
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