Chronic myeloid leukaemia articles within Nature

Featured

  • 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

  • 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 |

    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

  • 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

  • Outlook |

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

    • Emily Elert

  • Letter |

    Chronic myeloid leukaemia is caused by a BCR-ABL fusion, a constitutively active tyrosine kinase that, it is believed, leads to suppression of the forkhead O transcription factors (FOXO). Although the use of the tyrosine kinase inhibitor imatinib is a breakthrough for CML therapy, imatinib does not deplete the leukaemia-initiating cells (LICs) that drive the recurrence of CML. Foxo3a is now shown to have an essential role in the maintenance of CML LICs in a mouse model.

    • Kazuhito Naka
    • , Takayuki Hoshii
    •  & Atsushi Hirao

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