Haematological cancer articles within Nature

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  • 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 |

    Thalidomide and its derivative lenalidomide bind the CRL4CRBN E3 ubiquitin ligase and target protein substrates for degradation; structural and functional data determined here show that casein kinase 1α and the lymphoid transcription factor Ikaros, the efficacy targets of lenalidomide in two different blood cancers, interact with the CRBN–lenalidomide interface through a β-hairpin destruction motif.

    • Georg Petzold
    • , Eric S. Fischer
    •  & Nicolas H. Thomä

  • 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

  • Article |

    Lenalidomide, a derivative of thalidomide, is an effective drug for myelodysplastic syndrome; lenalidomide binds the CRL4CRBN E3 ubiquitin ligase and promotes degradation of casein kinase 1a, on which the malignant cells rely for survival.

    • Jan Krönke
    • , Emma C. Fink
    •  & Benjamin L. Ebert

  • 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 |

    Inactivation of the S1PR2–Gα13–ARHGEF1 signalling pathway in mice allows Akt activation and promotes dissemination of germinal centre B cells, consistent with a role of function-disrupting mutations in the systemic dissemination of diffuse large B-cell lymphoma.

    • Jagan R. Muppidi
    • , Roland Schmitz
    •  & Jason G. Cyster

  • 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

  • Article |

    The crystal structures of thalidomide and its derivatives bound to the E3 ligase subcomplex DDB1–CRBN are shown; these drugs are found to have dual functions, interfering with the binding of certain cellular substrates to the E3 ligase but promoting the binding of others, thereby modulating the degradation of cellular proteins.

    • Eric S. Fischer
    • , Kerstin Böhm
    •  & Nicolas H. Thomä

  • Letter |

    Global transcriptional and epigenomic analyses in diverse cell types reveal that the primary action of Myc is to up- and downregulate transcription of distinct groups of genes, rather than to amplify transcription of all active genes; general RNA amplification, when observed, is better explained as an indirect consequence of Myc’s action on cellular physiology.

    • Arianna Sabò
    • , Theresia R. Kress
    •  & Bruno Amati

  • 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

  • Article |

    T cells develop from thymic precursor cells that are constantly replaced with newly arriving bone marrow progenitor cells, and the ‘old’ and ‘new’ cells are shown here to compete; in the absence of cell competition, when the influx of new bone marrow progenitor cells is blocked, the old cells acquire the ability to self-renew and eventually become transformed, leading to the development of a form of leukaemia.

    • Vera C. Martins
    • , Katrin Busch
    •  & Hans-Reimer Rodewald

  • Letter |

    In mice with Eµ-myc transgenic lymphomas in which therapy-induced senescence (TIS) depends on the H3K9 histone methyltransferase Suv39h1, TIS-competent lymphomas but not TIS-incompetent Suv39h1– lymphomas show increased glucose utilization and ATP production after senescence-inducing chemotherapy to cope with proteotoxic stress elicited by factors of the senescence-associated secretory phenotype (SASP); senescent cancers are selectively vulnerable to drugs that block glucose utilization or autophagy.

    • Jan R. Dörr
    • , Yong Yu
    •  & Clemens A. Schmitt

  • Outlook |

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

    • Emily Elert

  • Outlook |

    Bruce L. Levine and Carl H. June explore how to make engineered immune cells that can eradicate cancer widely available.

    • Bruce L. Levine
    •  & Carl H. June

  • Outlook |

    Enzymes that modify gene expression without changing the DNA sequence are now viewed as central to the development of leukaemia — and may lead to new drugs.

    • Jessica Wright

  • Outlook |

    Leukaemia treatments must eliminate the versatile cells that can bring the cancer back to life years later.

    • Cassandra Willyard

  • Outlook |

    Leukaemia in children is highly curable, but many survivors suffer severe, even life-threatening, long-term effects. Scientists are seeking ways to deliver a safer cure.

    • Mary Carmichael

  • Outlook |

    Beginning treatment with a combination of drugs should help to stop drug resistance developing, says Charles L. Sawyers.

    • Charles L. Sawyers

  • Outlook |

    Stem cells from the umbilical cord are among the latest weapons in the fight against leukaemia.

    • Melinda Wenner Moyer

  • Outlook |

    Better designs for clinical trials and the use of combination therapies may improve leukaemia treatment.

    • Alla Katsnelson

  • Outlook |

    Technologies that rapidly sequence DNA reveal deep genetic diversity both within and among individuals with leukaemia.

    • Sarah DeWeerdt

  • Letter |

    EZH2 is a methyltransferase that is mutated in lymphoma; here a potent small molecule inhibitor of EZH2 is described, which inhibits the proliferation of EZH2 mutant cell lines and growth of EZH2 mutant xenografts in mice, thus providing a potential treatment for EZH2 mutant lymphoma.

    • Michael T. McCabe
    • , Heidi M. Ott
    •  & Caretha L. Creasy

  • Letter |

    B-cell receptor (BCR) signalling in chronic lymphocytic leukaemia (CLL) is found not to be dependent on exogenous antigens; instead, signalling may involve the binding of the BCR heavy-chain complementarity-determining region to self epitopes on the same receptor, a finding that may have important implications for understanding the pathogenesis of CLL and potential therapeutic approaches.

    • Marcus Dühren-von Minden
    • , Rudolf Übelhart
    •  & Hassan Jumaa

  • Outlook |

    Unlocking the genetic secrets of multiple myeloma could reveal new ways to attack this killer disease.

    • Courtney Humphries

  • Outlook |

    Identifying the patients most likely to progress from a precancerous condition to multiple myeloma could help doctors catch the disease early and stop it taking hold.

    • Lauren Gravitz

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