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Transformation from committed progenitor to leukaemia stem cell initiated by MLL–AF9

Author

Listed:
  • Andrei V. Krivtsov

    (Children's Hospital)

  • David Twomey

    (Children's Hospital
    The Broad Institute of Harvard and MIT)

  • Zhaohui Feng

    (Department of Pediatric Oncology)

  • Matthew C. Stubbs

    (Children's Hospital)

  • Yingzi Wang

    (Children's Hospital)

  • Joerg Faber

    (Children's Hospital)

  • Jason E. Levine

    (Children's Hospital
    Department of Pediatric Oncology)

  • Jing Wang

    (Department of Pediatric Oncology)

  • William C. Hahn

    (Medical Oncology, Dana Farber Cancer Institute
    The Broad Institute of Harvard and MIT)

  • D. Gary Gilliland

    (Brigham and Women's Hospital, Harvard Medical School
    Howard Hughes Medical Institute)

  • Todd R. Golub

    (Department of Pediatric Oncology
    The Broad Institute of Harvard and MIT
    Howard Hughes Medical Institute)

  • Scott A. Armstrong

    (Children's Hospital
    Department of Pediatric Oncology)

Abstract

Identity of cancer stem cells Cancer is thought to arise either from normal tissue cells or committed progenitors. A key question is how in the latter case cancer stem cells with the ability to self-renew — a property lacking in progenitor cells — can arise. A population of mouse leukaemia stem cells capable of initiating leukaemia when as few as four cells are injected into recipient mice has now been isolated from mice in which leukaemia arises through a mutation in committed progenitor cells. This made it possible to use gene expression profiling to determine global cellular identity and to view the transition from normal progenitor to leukaemia stem cell. Remarkably, the leukaemia stem cell largely maintains the gene expression profile of a committed progenitor, while activating a subset of genes normally expressed in haematopoietic stem cells. At least some of these genes are important for self-renewal in the leukaemic stem cells. The differences between leukaemic and normal blood stem cells may also be good news for the prospects of developing a drug that selectively targets cancer stem cells.

Suggested Citation

  • Andrei V. Krivtsov & David Twomey & Zhaohui Feng & Matthew C. Stubbs & Yingzi Wang & Joerg Faber & Jason E. Levine & Jing Wang & William C. Hahn & D. Gary Gilliland & Todd R. Golub & Scott A. Armstron, 2006. "Transformation from committed progenitor to leukaemia stem cell initiated by MLL–AF9," Nature, Nature, vol. 442(7104), pages 818-822, August.
    • Handle: RePEc:nat:nature:v:442:y:2006:i:7104:d:10.1038_nature04980
    DOI: 10.1038/nature04980
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    Cited by:

    1. Georgia K. Atkin-Smith & Jascinta P. Santavanond & Amanda Light & Joel S. Rimes & Andre L. Samson & Jeremy Er & Joy Liu & Darryl N. Johnson & Mélanie Le Page & Pradeep Rajasekhar & Raymond K. H. Yip &, 2024. "In situ visualization of endothelial cell-derived extracellular vesicle formation in steady state and malignant conditions," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    2. Yan, Kexun & Wang, Maoxiang & Hu, Fenglan & Xu, Meng, 2023. "Effect of cellular dedifferentiation on the growth of cell lineages," Physica A: Statistical Mechanics and its Applications, Elsevier, vol. 632(P1).
    3. Qianze Dong & Yan Xiu & Yang Wang & Christina Hodgson & Nick Borcherding & Craig Jordan & Jane Buchanan & Eric Taylor & Brett Wagner & Mariah Leidinger & Carol Holman & Dennis J. Thiele & Sean O’Brien, 2022. "HSF1 is a driver of leukemia stem cell self-renewal in acute myeloid leukemia," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    4. Raquel S. Pereira & Rahul Kumar & Alessia Cais & Lara Paulini & Alisa Kahler & Jimena Bravo & Valentina R. Minciacchi & Theresa Krack & Eric Kowarz & Costanza Zanetti & Parimala Sonika Godavarthy & Fa, 2023. "Distinct and targetable role of calcium-sensing receptor in leukaemia," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    5. Ian G. Cowell & Caroline A. Austin, 2012. "Mechanism of Generation of Therapy Related Leukemia in Response to Anti-Topoisomerase II Agents," IJERPH, MDPI, vol. 9(6), pages 1-17, May.

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