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Bloehdorn, Johannes; Braun, Andrejs; Taylor-Weiner, Amaro; Jebaraj, Billy Michael Chelliah; Robrecht, Sandra; Krzykalla, Julia; Pan, Heng; Giza, Adam; Akylzhanova, Gulnara; Holzmann, Karlheinz; Scheffold, Annika; Johnston, Harvey E; Yeh, Ru-Fang; Klymenko, Tetyana; Tausch, Eugen; Eichhorst, Barbara; Bullinger, Lars; Fischer, Kirsten; Weisser, Martin; Robak, Tadeusz; Schneider, Christof; Gribben, John; Dahal, Lekh N; Carter, Mathew J; Elemento, Olivier; Landau, Dan A; Neuberg, Donna S; Cragg, Mark S; Benner, Axel; Hallek, Michael; Wu, Catherine J; Döhner, Hartmut; Stilgenbauer, Stephan; Mertens, Daniel
Nature communications, 09/2021, Letnik: 12, Številka: 1Journal Article
Knowledge of the genomic landscape of chronic lymphocytic leukemia (CLL) grows increasingly detailed, providing challenges in contextualizing the accumulated information. To define the underlying networks, we here perform a multi-platform molecular characterization. We identify major subgroups characterized by genomic instability (GI) or activation of epithelial-mesenchymal-transition (EMT)-like programs, which subdivide into non-inflammatory and inflammatory subtypes. GI CLL exhibit disruption of genome integrity, DNA-damage response and are associated with mutagenesis mediated through activation-induced cytidine deaminase or defective mismatch repair. TP53 wild-type and mutated/deleted cases constitute a transcriptionally uniform entity in GI CLL and show similarly poor progression-free survival at relapse. EMT-like CLL exhibit high genomic stability, reduced benefit from the addition of rituximab and EMT-like differentiation is inhibited by induction of DNA damage. This work extends the perspective on CLL biology and risk categories in TP53 wild-type CLL. Furthermore, molecular targets identified within each subgroup provide opportunities for new treatment approaches.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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