Journal
CANCER CELL
Volume 30, Issue 6, Pages 849-862Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2016.11.002
Keywords
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Funding
- ERC [681524]
- Deutsche Jose Carreras Leukamie-Stiftung [R 10/26]
- Collaborative Research Centers 684 Molecular Mechanisms of Normal and Malignant Hematopoiesis [1243]
- German Consortium for Translational Cancer Research (DKTK)
- Bettina Brau-Stiftung
- Dr. Helmut Legerlotz Stiftung
- Collaborative Research Center 1243, project A14
- German Federal Ministry of Education and Research (BMBF) within the Virtual Liver Project [0315766]
- German Research Foundation [SPP1395/InKoMBio Busch 900/6-1]
- DFG [GI-540-3/1]
- [07]
- [08]
- European Research Council (ERC) [681524] Funding Source: European Research Council (ERC)
- Cancer Research UK [12796] Funding Source: researchfish
- Great Ormond Street Hospital Childrens Charity [W1062] Funding Source: researchfish
- Medical Research Council [MR/N000838/1, G1000801g, MR/M009033/1] Funding Source: researchfish
- MRC [MR/M009033/1, MR/N000838/1] Funding Source: UKRI
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Tumor relapse is associated with dismal prognosis, but responsible biological principles remain incompletely understood. To isolate and characterize relapse-inducing cells, we used genetic engineering and proliferation-sensitive dyes in patient-derived xenografts of acute lymphoblastic leukemia (ALL). We identified a rare subpopulation that resembled relapse-inducing cells with combined properties of long-term dormancy, treatment resistance, and stemness. Single-cell and bulk expression profiling revealed their similarity to primary ALL cells isolated from pediatric and adult patients at minimal residual disease (MRD). Therapeutically adverse characteristics were reversible, as resistant, dormant cells became sensitive to treatment and started proliferating when dissociated from the in vivo environment. Our data suggest that ALL patients might profit from therapeutic strategies that release MRD cells from the niche.
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