dc.contributor.author | Bloehdorn, J | |
dc.contributor.author | Braun, A | |
dc.contributor.author | Taylor-Weiner, A | |
dc.contributor.author | Jebaraj, BMC | |
dc.contributor.author | Robrecht, S | |
dc.contributor.author | Krzykalla, J | |
dc.contributor.author | Pan, H | |
dc.contributor.author | Giza, A | |
dc.contributor.author | Akylzhanova, G | |
dc.contributor.author | Holzmann, K | |
dc.contributor.author | Scheffold, A | |
dc.contributor.author | Johnston, HE | |
dc.contributor.author | Yeh, R-F | |
dc.contributor.author | Klymenko, T | |
dc.contributor.author | Tausch, E | |
dc.contributor.author | Eichhorst, B | |
dc.contributor.author | Bullinger, L | |
dc.contributor.author | Fischer, K | |
dc.contributor.author | Weisser, M | |
dc.contributor.author | Robak, T | |
dc.contributor.author | Schneider, C | |
dc.contributor.author | Gribben, J | |
dc.contributor.author | Dahal, LN | |
dc.contributor.author | Carter, MJ | |
dc.contributor.author | Elemento, O | |
dc.contributor.author | Landau, DA | |
dc.contributor.author | Neuberg, DS | |
dc.contributor.author | Cragg, MS | |
dc.contributor.author | Benner, A | |
dc.contributor.author | Hallek, M | |
dc.contributor.author | Wu, CJ | |
dc.contributor.author | Döhner, H | |
dc.contributor.author | Stilgenbauer, S | |
dc.contributor.author | Mertens, D | |
dc.date.accessioned | 2021-09-17T14:00:56Z | |
dc.date.available | 2021-09-17T14:00:56Z | |
dc.date.issued | 2021-12 | |
dc.identifier.citation | Bloehdorn, J., Braun, A., Taylor-Weiner, A. et al. Multi-platform profiling characterizes molecular subgroups and resistance networks in chronic lymphocytic leukemia. Nat Commun 12, 5395 (2021). https://doi.org/10.1038/s41467-021-25403-y | en_US |
dc.identifier.other | 5395 | |
dc.identifier.uri | https://qmro.qmul.ac.uk/xmlui/handle/123456789/74103 | |
dc.description.abstract | 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. | en_US |
dc.language | en | |
dc.language.iso | en | en_US |
dc.publisher | Springer Science and Business Media LLC | en_US |
dc.relation.ispartof | Nature Communications | |
dc.rights | Creative Commons Attribution 4.0 International License | |
dc.title | Multi-platform profiling characterizes molecular subgroups and resistance networks in chronic lymphocytic leukemia | en_US |
dc.type | Article | en_US |
dc.rights.holder | © The Author(s) 2021 | |
dc.identifier.doi | 10.1038/s41467-021-25403-y | |
pubs.issue | 1 | en_US |
pubs.notes | Not known | en_US |
pubs.publication-status | Published online | en_US |
pubs.volume | 12 | en_US |
rioxxterms.funder | Default funder | en_US |
rioxxterms.identifier.project | Default project | en_US |