ArticleEMBO molecular medicine2012
Diverging fates of cells of origin in acute and chronic leukaemia.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Tumor Microenvironment: A Niche for Cancer Stem Cell Immunotherapy.Stem cell reviews and reports · 2024Review
- RHOA-regulated IGFBP2 promotes invasion and drives progression of BCR-ABL1 chronic myeloid leukemia.Haematologica · 2023Article
- Review
- Characterization of p190-Bcr-Abl chronic myeloid leukemia reveals specific signaling pathways and therapeutic targets.Leukemia · 2021Article
- Forward and Reverse Genetics of B Cell Malignancies: From Insertional Mutagenesis to CRISPR-Cas.Frontiers in immunology · 2021Review
- Global gene expression profiles of hematopoietic stem and progenitor cells from patients with chronic myeloid leukemia: the effect of in vitro culture with or without imatinib.Cancer medicine · 2017Article
- Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis.Leukemia · 2017Article
- Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics.Leukemia · 2017Article
- SOCS1 function in BCR-ABL mediated myeloproliferative disease is dependent on the cytokine environment.PloS one · 2017Article
- The target cell of transformation is distinct from the leukemia stem cell in murine CALM/AF10 leukemia models.Leukemia · 2016Article
- Article
- Review
- STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.Oncotarget · 2012Article
- Modeling ETV6-JAK2-induced leukemia: insights from the zebrafish.Haematologica · 2012Article
- Lineage switching in acute leukemias: a consequence of stem cell plasticity?Bone marrow research · 2012Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The large difference in phenotypes among tumour populations may stem from the stochastic origin of tumours from distinct cells - tumour cells are assumed to retain the phenotypes of the cells from which they derive. Yet, functional studies addressing the cellular origin of leukaemia are lacking. Here we show that the cells of origin of both, BCR/ABL-induced chronic myeloid (CML) and B-cell acute lymphoid leukaemia (B-ALL), resemble long-term haematopoietic stem cells (LT-HSCs). During disease-maintenance, CML LT-HSCs persist to function as cancer stem cells (CSCs) that maintain leukaemia and require signalling by the transcription factor STAT5. In contrast, B-ALL LT-HSCs differentiate into CSCs that correspond to pro-B cells. This transition step requires a transient IL-7 signal and is lost in IL-7Rα-deficient cells. Thus, in BCR/ABLp185(+) B-ALL and BCR/ABLp210(+) CML, the final phenotype of the tumour as well as the abundance of CSCs is dictated by diverging differentiation fates of their common cells of origin.
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