ArticleBlood2012
Bmi1 reprograms CML B-lymphoid progenitors to become B-ALL-initiating cells.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- The nutrigenomic-epigenetic axis in cancer: from dietary bioactives to precision oncology.Nutrition & metabolism · 2026Review
- A characteristic gene expression profile regulated by ACIN1::NUTM1 fusion in a newly identified infant leukaemic cell line and an ACIN1::NUTM1-inducible model.British journal of haematology · 2025Article
- Nuclear Vav3 is required for polycomb repression complex-1 activity in B-cell lymphoblastic leukemogenesis.Nature communications · 2022Article
- Integrating genetic and epigenetic factors in chronic myeloid leukemia risk assessment: toward gene expression-based biomarkers.Haematologica · 2022Review
- Article
- The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors.Nature communications · 2019Article
- Epigenetic Reprogramming and Emerging Epigenetic Therapies in CML.Frontiers in cell and developmental biology · 2019Review
- Stat5 deficiency decreases transcriptional heterogeneity and supports emergence of hematopoietic sub-populations.Oncotarget · 2017Article
- Modeling BCR-ABL and MLL-AF9 leukemia in a human bone marrow-like scaffold-based xenograft model.Leukemia · 2016Article
- CDKN2A-independent role of BMI1 in promoting growth and survival of Ph+ acute lymphoblastic leukemia.Leukemia · 2016Article
- The roles of Polycomb group proteins in hematopoietic stem cells and hematological malignancies.International journal of hematology · 2016Review
- Modeling of Chronic Myeloid Leukemia: An Overview of In Vivo Murine and Human Xenograft Models.Stem cells international · 2016Review
- BMI1: A Biomarker of Hematologic Malignancies.Biomarkers in cancer · 2016Review
- Clonal-level responses of functionally distinct hematopoietic stem cells to trophic factors.Experimental hematology · 2014Article
- Synergy against PML-RARa: targeting transcription, proteolysis, differentiation, and self-renewal in acute promyelocytic leukemia.The Journal of experimental medicine · 2013Review
- Aberrant epigenetic regulators control expansion of human CD34+ hematopoietic stem/progenitor cells.Frontiers in genetics · 2013Review
- Polycomb-group proteins in hematopoietic stem cell regulation and hematopoietic neoplasms.Leukemia · 2013Review
- Vav3 collaborates with p190-BCR-ABL in lymphoid progenitor leukemogenesis, proliferation, and survival.Blood · 2012Article
- Pushing the limits of targeted therapy in chronic myeloid leukaemia.Nature reviews. Cancer · 2012Review
- Effects ofAvicenna journal of phytomedicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The characterization and targeting of Philadelphia chromosome positive (Ph(+)) acute lymphoblastic leukemia (ALL)-initiating cells remains unresolved. Expression of the polycomb protein Bmi1 is up-regulated in patients with advanced stages of chronic myelogenous leukemia (CML). We report that Bmi1 transforms and reprograms CML B-lymphoid progenitors into stem cell leukemia (Scl) promoter-driven, self-renewing, leukemia-initiating cells to result in B-lymphoid leukemia (B-ALL) in vivo. In vitro, highly proliferating and serially replatable myeloid and lymphoid colony-forming cultures could be established from BCR-ABL and Bmi1 coexpressing progenitors. However, unlike in vivo expanded CML B-lymphoid progenitors, hematopoietic stem cells, or multipotent progenitors, coexpressing BCR-ABL and Bmi1 did not initiate or propagate leukemia in a limiting dilution assay. Inducible genetic attenuation of BCR-ABL reversed Bmi1-driven B-ALL development, which was accompanied by induction of apoptosis of leukemic B-lymphoid progenitors and by long-term animal survival, suggesting that BCR-ABL is required to maintain B-ALL and that BCR-ABL and Bmi1 cooperate toward blast transformation in vivo. Our data indicate that BCR-ABL targeting itself is required to eradicate Ph(+)/Bmi1(+) B-ALL-initiating cells and confirm their addiction to BCR-ABL signaling.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.