Acute lymphocytic leukaemia articles within Nature

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  • 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

  • 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 |

    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

  • 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 |

    Leukaemias are cancers of the blood or bone marrow. But how do they form, and can they be treated?

    • Emily Elert

  • News & Views |

    Mutations that lead to increased activity of the Notch signalling pathway are well defined in human cancer. New work implicates decreased activity of this pathway in a type of blood cancer. See Letter p.230

    • Demetrios Kalaitzidis
    •  & Scott A. Armstrong

  • Letter |

    In three different subtypes of B-cell lymphomas, two papers now report frequent somatic mutations in CREBBP and EP300, present in primary tumours or acquired at relapse. These genes encode related acetyltransferases that mainly function to regulate gene expression by acetylating histones and other transcriptional regulators. The mutations found inactivate these activities and thus alter chromatin regulation of gene expression, as well as proliferation and potentially the response to therapeutic drugs.

    • Charles G. Mullighan
    • , Jinghui Zhang
    •  & James R. Downing

  • Article |

    Analysing single cells from human B-cell acute lymphoblastic leukaemias, this study maps the genetic heterogeneity of cells within a given tumour sample, the evolutionary path by which different subclones have emerged, and ongoing dynamic changes associated with relapse. Leukaemia-propagating cells that transplant the disease mirror the genetic variegation of the bulk tumours, providing insights into the heterogeneity of these functional subpopulations at the genetic level. This has implications for therapeutic approaches targeting the tumours and specifically leukaemia-propagating cells.

    • Kristina Anderson
    • , Christoph Lutz
    •  & Mel Greaves

  • Letter |

    The four receptors of the Notch family are transmembrane proteins through which mammalian cells communicate to regulate cell fate and growth. Aberrant signalling through each receptor has been linked to disease, so the Notch pathway is a compelling drug target. But current drugs cannot distinguish between the different Notch proteins. Here, phage display technology has been used to generate highly specialized antibodies, enabling the functions of Notch1 and Notch2 to be discriminated in humans and mice.

    • Yan Wu
    • , Carol Cain-Hom
    •  & Christian W. Siebel

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