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@ARTICLE{Costea:302323,
      author       = {J. Costea and K. K. Rauwolf and P. Zafferani$^*$ and T.
                      Rausch and A. Mathioudaki$^*$ and J. Zaugg and M. Schrappe
                      and C. Eckert$^*$ and G. Escherich and J. P. Bourquin and B.
                      Bornhauser and A. Kulozik$^*$ and J. Korbel$^*$},
      title        = {{R}ole of stem-like cells in chemotherapy resistance and
                      relapse in pediatric {T}-cell acute lymphoblastic leukemia.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01318},
      pages        = {5413},
      year         = {2025},
      note         = {#LA:B480#},
      abstract     = {T-ALL relapses are characterized by chemotherapy
                      resistance, cellular diversity and dismal outcome. To gain a
                      deeper understanding of the mechanisms underlying relapses,
                      we conduct single-cell RNA sequencing on 13 matched
                      pediatric T-ALL patient-derived samples at diagnosis and
                      relapse, along with samples derived from 5 non-relapsing
                      patients collected at diagnosis. This comprehensive
                      longitudinal single-cell study in T-ALL reveals significant
                      transcriptomic diversity. Notably, 11 out of 18 samples
                      exhibit a subpopulation of T-ALL cells with stem-like
                      features characterized by a common set of active regulons,
                      expression patterns and splice isoforms. This subpopulation,
                      accounting for a small proportion of leukemia cells at
                      diagnosis, expands substantially at relapse, indicating
                      resistance to therapy. Strikingly, increased stemness at
                      diagnosis is associated with higher risk of treatment
                      induction failure. Chemotherapy resistance is validated
                      through in-vitro and in-vivo drug testing. Thus, we report
                      the discovery of treatment-resistant stem-like cells in
                      T-ALL, underscoring the potential for devising future
                      therapeutic strategies targeting stemness-related pathways.},
      keywords     = {Humans / Drug Resistance, Neoplasm: genetics / Precursor
                      T-Cell Lymphoblastic Leukemia-Lymphoma: drug therapy /
                      Precursor T-Cell Lymphoblastic Leukemia-Lymphoma: genetics /
                      Precursor T-Cell Lymphoblastic Leukemia-Lymphoma: pathology
                      / Child / Neoplastic Stem Cells: metabolism / Neoplastic
                      Stem Cells: pathology / Neoplastic Stem Cells: drug effects
                      / Single-Cell Analysis / Male / Female / Child, Preschool /
                      Adolescent / Neoplasm Recurrence, Local: genetics /
                      Recurrence / Transcriptome / Animals / Mice / Cell Line,
                      Tumor / Gene Expression Regulation, Leukemic},
      cin          = {B270 / B450 / BE01 / A400 / B480},
      ddc          = {500},
      cid          = {I:(DE-He78)B270-20160331 / I:(DE-He78)B450-20160331 /
                      I:(DE-He78)BE01-20160331 / I:(DE-He78)A400-20160331 /
                      I:(DE-He78)B480-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40579412},
      doi          = {10.1038/s41467-025-61222-1},
      url          = {https://inrepo02.dkfz.de/record/302323},
}