% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Arseni:298222,
      author       = {L. Arseni$^*$ and G. Sigismondo$^*$ and H. Yazdanparast$^*$
                      and J. U. Hermansen and N. Mack$^*$ and S. Ohl$^*$ and V.
                      Kalter$^*$ and M. Iskar$^*$ and M. Kalxdorf and D.
                      Friedel$^*$ and M. Rettel and Y. Paul$^*$ and I. Ringshausen
                      and E. Eldering and J. Dubois and A. P. Kater and M.
                      Zapatka$^*$ and P. M. Roessner$^*$ and E. Tausch and S.
                      Stilgenbauer and S. Dietrich and M. M. Savitski and S. S.
                      Skånland and J. Krijgsveld$^*$ and P. Lichter$^*$ and M.
                      Seiffert$^*$},
      title        = {{L}ongitudinal omics data and preclinical treatment suggest
                      the proteasome inhibitor carfilzomib as therapy for
                      ibrutinib-resistant {CLL}.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-00229},
      pages        = {1041},
      year         = {2025},
      note         = {#EA:B060#EA:B230#LA:B060#},
      abstract     = {Chronic lymphocytic leukemia is a malignant
                      lymphoproliferative disorder for which primary or acquired
                      drug resistance represents a major challenge. To investigate
                      the underlying molecular mechanisms, we generate a mouse
                      model of ibrutinib resistance, in which, after initial
                      treatment response, relapse under therapy occurrs with an
                      aggressive outgrowth of malignant cells, resembling
                      observations in patients. A comparative analysis of exome,
                      transcriptome and proteome of sorted leukemic murine cells
                      during treatment and after relapse suggests alterations in
                      the proteasome activity as a driver of ibrutinib resistance.
                      Preclinical treatment with the irreversible proteasome
                      inhibitor carfilzomib administered upon ibrutinib resistance
                      prolongs survival of mice. Longitudinal proteomic analysis
                      of ibrutinib-resistant patients identifies deregulation in
                      protein post-translational modifications. Additionally,
                      cells from ibrutinib-resistant patients effectively respond
                      to several proteasome inhibitors in co-culture assays.
                      Altogether, our results from orthogonal omics approaches
                      identify proteasome inhibition as potentially attractive
                      treatment for chronic lymphocytic leukemia patients
                      resistant or refractory to ibrutinib.},
      keywords     = {Adenine: analogs $\&$ derivatives / Adenine: therapeutic
                      use / Adenine: pharmacology / Leukemia, Lymphocytic,
                      Chronic, B-Cell: drug therapy / Leukemia, Lymphocytic,
                      Chronic, B-Cell: genetics / Leukemia, Lymphocytic, Chronic,
                      B-Cell: metabolism / Piperidines: pharmacology /
                      Piperidines: therapeutic use / Animals / Humans / Proteasome
                      Inhibitors: pharmacology / Proteasome Inhibitors:
                      therapeutic use / Drug Resistance, Neoplasm: genetics / Drug
                      Resistance, Neoplasm: drug effects / Oligopeptides:
                      pharmacology / Oligopeptides: therapeutic use / Mice /
                      Pyrimidines: pharmacology / Pyrimidines: therapeutic use /
                      Pyrazoles: pharmacology / Pyrazoles: therapeutic use /
                      Proteomics / Proteasome Endopeptidase Complex: metabolism /
                      Disease Models, Animal / Female / Cell Line, Tumor /
                      ibrutinib (NLM Chemicals) / carfilzomib (NLM Chemicals) /
                      Adenine (NLM Chemicals) / Piperidines (NLM Chemicals) /
                      Proteasome Inhibitors (NLM Chemicals) / Oligopeptides (NLM
                      Chemicals) / Pyrimidines (NLM Chemicals) / Pyrazoles (NLM
                      Chemicals) / Proteasome Endopeptidase Complex (NLM
                      Chemicals)},
      cin          = {B060 / B230 / B300},
      ddc          = {500},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)B230-20160331 /
                      I:(DE-He78)B300-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39863584},
      pmc          = {pmc:PMC11762753},
      doi          = {10.1038/s41467-025-56318-7},
      url          = {https://inrepo02.dkfz.de/record/298222},
}