ArticleMolecular and cellular biology2004
Roles of Bim in apoptosis of normal and Bcr-Abl-expressing hematopoietic progenitors.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 152 citations in OpenAlex.
- MEK1/2 inhibitors sensitize Bcr/Abl+ human leukemia cells to the dual Abl/Src inhibitor BMS-354/825.Blood · 2007Trial
- Differential mitochondrial priming by BCR::ABL1 in B-cell precursor acute lymphoblastic leukemia.Leukemia · 2026Article
- Multimodal gene and targeted drug therapy for chronic myelogenous leukemia using BIM/MCL-1 chimeric nanoparticle: computational target analysis and therapeutic validation.Nano convergence · 2026Article
- Cytogenetic and molecular characterization of an atypical ETP-ALL case with BCL2 dependency: therapeutic implications for Venetoclax use.Molecular biology reports · 2025Article
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- BH3 mimetics in combination with nilotinib or ponatinib represent a promising therapeutic strategy in blast phase chronic myeloid leukemia.Cell death discovery · 2022Article
- The application of BH3 mimetics in myeloid leukemias.Cell death & disease · 2021Review
- Systemic Mastocytosis: Molecular Landscape and Implications for Treatment.Mediterranean journal of hematology and infectious diseases · 2021Review
- Targeting apoptosis in cancer therapy.Nature reviews. Clinical oncology · 2020Review
- The polyphenol quercetin induces cell death in leukemia by targeting epigenetic regulators of pro-apoptotic genes.Clinical epigenetics · 2018Article
- Overcoming imatinib resistance conferred by theOncotarget · 2017Article
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- Cancer stem cells and chemoresistance: The smartest survives the raid.Pharmacology & therapeutics · 2016Review
- Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies.Nature reviews. Cancer · 2016Review
- The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia.Oncotarget · 2016Article
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- The BCL-2 protein family, BH3-mimetics and cancer therapy.Cell death and differentiation · 2015Review
- The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics.Cancer discovery · 2015Review
- A Translational, Pharmacodynamic, and Pharmacokinetic Phase IB Clinical Study of Everolimus in Resectable Non-Small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bcr-Abl kinase is known to reverse apoptosis of cytokine-dependent cells due to cytokine deprivation, although it has been controversial whether chronic myeloid leukemia (CML) progenitors have the potential to survive under conditions in which there are limited amounts of cytokines. Here we demonstrate that early hematopoietic progenitors (Sca-1(+) c-Kit(+) Lin(-)) isolated from normal mice rapidly undergo apoptosis in the absence of cytokines. In these cells, the expression of Bim, a proapoptotic relative of Bcl-2 which plays a key role in the cytokine-mediated survival system, is induced. In contrast, those cells isolated from our previously established CML model mice resist apoptosis in cytokine-free medium without the induction of Bim expression, and these effects are reversed by the Abl-specific kinase inhibitor imatinib mesylate. In addition, the expression levels of Bim are uniformly low in cell lines established from patients in the blast crisis phase of CML, and imatinib induced Bim in these cells. Moreover, small interfering RNA that reduces the expression level of Bim effectively rescues CML cells from apoptosis caused by imatinib. These findings suggest that Bim plays an important role in the apoptosis of early hematopoietic progenitors and that Bcr-Abl supports cell survival in part through downregulation of this cell death activator.
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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.