期刊
LEUKEMIA
卷 31, 期 12, 页码 2577-2586出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2017.140
关键词
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资金
- CRUK programme Grant [C27943/A12788]
- North of England Children's Cancer Research Fund
- Wellcome Trust [087961]
- MRC Clinical Research Training Fellowship [G0802259]
- NIHR Academic Clinical Lectureship
- Gordon Piller Studentship from Bloodwise [11042]
- Newcastle Healthcare Charity
- JGW Patterson Foundation fellowship
- MRC [G0802259] Funding Source: UKRI
- Cancer Research UK [23389, 12788] Funding Source: researchfish
- Medical Research Council [G0802259] Funding Source: researchfish
- National Institute for Health Research [CL-2012-01-002] Funding Source: researchfish
High frequencies of blasts in primary acute lymphoblastic leukaemia (ALL) samples have the potential to induce leukaemia and to engraft mice. However, it is unclear how individual ALL cells each contribute to drive leukaemic development in a bulk transplant and the extent to which these blasts vary functionally. We used cellular barcoding as a fate mapping tool to track primograft ALL blasts in vivo. Our results show that high numbers of ALL founder cells contribute at similar frequencies to leukaemic propagation over serial transplants, without any clear evidence of clonal succession. These founder cells also exhibit equal capacity to home and engraft to different organs, although stochastic processes may alter the composition in restrictive niches. Our findings enhance the stochastic stem cell model of ALL by demonstrating equal functional abilities of singular ALL blasts and show that successful treatment strategies must eradicate the entire leukaemic cell population.
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