Leukaemia articles within Nature

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  • Article
    | Open Access

    Epitope engineering of donor haematopoietic stem/progenitor cells endows haematopoietic lineages with selective resistance to CAR T cells or monoclonal antibodies, without affecting protein function or regulation, enabling the targeting of genes that are essential for leukaemia survival and reducing the risk of tumour immune escape.

    • Gabriele Casirati
    • , Andrea Cosentino
    •  & Pietro Genovese

  • Article
    | Open Access

    Blastic plasmacytoid dendritic cell neoplasm (BPDCN) arises from clonal (premalignant) haematopoietic precursors in the bone marrow, and BPDCN skin tumours first develop at sun-exposed anatomical sites and are distinguished by clonally expanded mutations induced by ultraviolet radiation.

    • Gabriel K. Griffin
    • , Christopher A. G. Booth
    •  & Andrew A. Lane

  • Article
    | Open Access

    Revumenib, a potent and selective oral inhibitor of the menin–KMT2A interaction, is associated with a low frequency of treatment-related adverse events and promising clinical activity in patients with relapsed or refractory acute leukaemia.

    • Ghayas C. Issa
    • , Ibrahim Aldoss
    •  & Eytan M. Stein

  • Article |

    Extensive genomic analyses of the chromatin architecture in acute myeloid leukaemia reveals several characteristics, including subtype-specific distal enhancers and silencers, that may represent new anticancer therapeutic targets.

    • Jie Xu
    • , Fan Song
    •  & Feng Yue

  • Article |

    Analysis of B-cell leukaemia samples reveals that oncogenic mutations do not cause malignant transformation unless they converge on the same signalling pathway, and that it may be possible clinically to combine inhibition of the principal oncogenic driver with reactivation of divergent pathways.

    • Lai N. Chan
    • , Mark A. Murakami
    •  & Markus Müschen

  • Article |

    The MYST acetyltransferase HBO1 is a critical regulator in maintaining leukaemia stem cells, and a small-molecule inhibitor of HBO1 is developed that shows efficacy against a range of acute myeloid leukaemia cells.

    • Laura MacPherson
    • , Juliana Anokye
    •  & Mark A. Dawson

  • Article |

    Analysis of growth dynamics in a dataset from 107 patients with chronic lymphocytic leukaemia (CLL) reveals both exponential and logistic patterns of growth, which are associated with differences in genetic attributes and clinical outcomes.

    • Michaela Gruber
    • , Ivana Bozic
    •  & Catherine J. Wu

  • Letter |

    A single-cell approach is used to follow the heritable stochastic changes to DNA methylation that occur in primary chronic lymphocytic leukaemia and healthy B cells, allowing the tracing of cell lineage histories and evolution during treatment with ibrutinib.

    • Federico Gaiti
    • , Ronan Chaligne
    •  & Dan A. Landau

  • Article |

    Analyses of samples from patients with acute myeloid leukaemia reveal that drug response is associated with mutational status and gene expression; the generated dataset provides a basis for future clinical and functional studies of this disease.

    • Jeffrey W. Tyner
    • , Cristina E. Tognon
    •  & Brian J. Druker

  • Article |

    A large-scale genomics study shows that the cell of origin and founding mutations determine disease subtype and lead to the expression of multiple haematopoietic lineage-defining antigens in mixed phenotype acute leukaemia.

    • Thomas B. Alexander
    • , Zhaohui Gu
    •  & Charles G. Mullighan

  • Letter |

    A crystal structure of DNMT3A and its regulatory partner DNMT3L bound to DNA reveals the mechanistic basis for DNMT3A-mediated DNA methylation and establishes its aetiological link to human disease.

    • Zhi-Min Zhang
    • , Rui Lu
    •  & Jikui Song

  • Letter |

    Mutations in the nucleotidase-encoding gene NT5C2 drive chemotherapy resistance in relapsed acute lymphoid leukaemia but the mutations also lead to a loss-of-fitness phenotype and to collateral drug sensitivity, which could be exploited for therapy.

    • Gannie Tzoneva
    • , Chelsea L. Dieck
    •  & Adolfo A. Ferrando

  • Article |

    During emergency myelopoiesis in mice, clusters of self-renewing granulocyte/macrophage progenitors (GMP) are transiently formed in the bone marrow cavity to produce a burst of myeloid cells; in leukaemia, GMP clusters persist and constantly generate myeloid leukaemia cells.

    • Aurélie Hérault
    • , Mikhail Binnewies
    •  & Emmanuelle Passegué

  • Letter |

    The selective allosteric ABL1 inhibitor ABL001 (asciminib) represents a new inhibitory mechanism for BCR–ABL1-driven malignancies, and its efficacy and evolving mechanisms of resistance do not overlap with those of other BCR–ABL1 kinase inhibitors.

    • Andrew A. Wylie
    • , Joseph Schoepfer
    •  & William R. Sellers

  • Letter |

    ENL, identified in a genome-scale loss-of-function screen as a crucial requirement for proliferation of acute leukaemia, is required for leukaemic gene expression, and its YEATS chromatin-reader domain is essential for leukaemic growth.

    • Michael A. Erb
    • , Thomas G. Scott
    •  & James E. Bradner

  • Letter |

    A rapid gene signature test (LSC17) that captures stem cell expression programs in acute myeloid leukaemia patients at diagnosis is associated with therapy response and survival, facilitating initial treatment stratification.

    • Stanley W. K. Ng
    • , Amanda Mitchell
    •  & Jean C. Y. Wang

  • Article |

    Leukaemic stem cells (LSCs) are responsible for BCR–ABL-driven chronic myeloid leukaemia relapse; here, p53 and MYC signalling networks are shown to regulate LSCs concurrently, and targeting both these pathways has a synergistic effect in managing the disease.

    • Sheela A. Abraham
    • , Lisa E. M. Hopcroft
    •  & Tessa L. Holyoake

  • Letter |

    A small-molecule inhibitor of the Mediator-associated kinases CDK8 and CDK19 inhibits growth of acute myeloid leukaemia (AML) cells and induces upregulation of super-enhancer-associated genes with tumour suppressor and lineage-controlling functions; Mediator kinase inhibition therefore represents a promising therapeutic approach for AML.

    • Henry E. Pelish
    • , Brian B. Liau
    •  & Matthew D. Shair

  • Letter |

    BET inhibitors that target bromodomain chromatin readers such as BRD4 are being explored as potential therapeutics in cancer; here, in a MLL–AF9 mouse leukaemia model, resistance to BET inhibitors is shown to emerge from leukaemia stem cells, and be partly due to increased Wnt/β-catenin signalling.

    • Chun Yew Fong
    • , Omer Gilan
    •  & Mark A. Dawson

  • Letter |

    BET bromodomain inhibitors are being explored as potential therapeutics in cancer; here, AML cells are shown to evade sensitivity to BET inhibition through rewiring the transcriptional regulation of BRD4 target genes such as MYC in a process that is facilitated by suppression of PRC2 and WNT signalling activation.

    • Philipp Rathert
    • , Mareike Roth
    •  & Johannes Zuber

  • Letter |

    Although imatinib gives good clinical results in chronic myeloid leukaemia (CML), residual disease attributed to quiescent CML stem cells remains in many patients; here glitazones are shown to reduce the pool of CML stem cells and achieve lasting disease eradication in CML patients in combination with imatinib.

    • Stéphane Prost
    • , Francis Relouzat
    •  & Philippe Leboulch

  • Letter |

    This study shows that, despite malignant transformation, autoimmune checkpoints are still functional in B-cell leukaemia, with targeted activation of these checkpoints effectively killing patient-derived B-cell leukaemia in a transplant model; the results represent a novel strategy to overcome drug resistance in leukaemia patients.

    • Zhengshan Chen
    • , Seyedmehdi Shojaee
    •  & Markus Müschen

  • Letter |

    Somatic TP53 mutations are highly prevalent in therapy-related acute myeloid leukaemia and myelodysplastic syndrome, which arise as complications of cytotoxic chemotherapy or radiotherapy; although it was believed that these TP53 mutations are directly induced by cytotoxic therapy, new data indicate that they predate cytotoxic therapy and that haematopoietic progenitors harbouring these pre-existing mutations may selectively expand after exposure to chemotherapy or radiotherapy.

    • Terrence N. Wong
    • , Giridharan Ramsingh
    •  & Richard K. Wilson

  • Letter |

    T-cell acute lymphoblastic leukaemia (T-ALL) is a haematological malignancy with a poor prognosis and no available targeted therapies; now two histone H3 lysine 27 demethylases, JMJD3 and UTX, are shown to have contrasting roles in human T-ALL cells and a mouse model of the disease, and a small molecule demethylase inhibitor is found to inhibit the growth of T-ALL cell lines, introducing a potential therapeutic avenue for acute leukaemia.

    • Panagiotis Ntziachristos
    • , Aristotelis Tsirigos
    •  & Iannis Aifantis

  • Article |

    The translation of many messenger RNAs that encode important oncogenes and transcription factors depends on the eIF4A RNA helicase to resolve G-quadruplex structures, implying eIF4A inhibition as an effective cancer therapy.

    • Andrew L. Wolfe
    • , Kamini Singh
    •  & Hans-Guido Wendel

  • Outlook |

    Tailoring cancer treatment to individual and evolving tumours is the way of the future, but scientists are still hashing out the details.

    • Lauren Gravitz

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