ArticleCell stem cell2013
BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells.
Article in Cell stem cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 858 papers.
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Who cites it
858 citing papers in PubMed.
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- Phase 2 study of chidamide in combination with CAG and venetoclax-azacitidine in older patients with newly diagnosed acute myeloid leukemia.Frontiers in immunology · 2025Trial
- Feasibility and Safety of Venetoclax for Cytoreduction During Induction Therapy in Newly Diagnosed Acute Promyelocytic Leukemia.European journal of haematology · 2026Article
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- Ptpn1 deficiency collaborates with a NUP98::HOXD13 fusion gene to generate B cell precursor acute lymphoblastic leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Pharmacological blockade of rho kinase enhances venetoclax responses in translational models of acute myeloid leukemia.Haematologica · 2026Article
- Non-genetic remodeling drives leukemia propagation and reveals actionable vulnerabilities in acute myeloid leukemia.Cell reports. Medicine · 2026Article
- AI-enabled multi-omics pharmacogenomic modeling guides resistance-aware multitarget optimization of venetoclax therapy in acute myeloid leukemia.NPJ precision oncology · 2026Article
- Glucose-induced histone lactylation confers metformin resistance in colorectal cancer stem cells.Nature communications · 2026Article
- Mitochondrial Fitness as a Functional Immune Checkpoint in Cancer: Metabolic Plasticity, Tumor Evolution, and Immunotherapy.Cancers · 2026Review
- Exploiting Metabolic Vulnerabilities in Acute Myeloid Leukemia: Rationale and Evidence for Combining Metabolic Modulators with Conventional Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Glutathione metabolism-linked ferroptosis in human seminoma: a spatial multi-omics mapping study.Redox biology · 2026Article
- Metabolic Reprogramming of Cancer Stem Cells: Targeting Lipid Flux and Mitochondrial Plasticity to Overcome Therapeutic Resistance.Cancer medicine · 2026Review
- Targeting ClpP Protease: Emerging Therapeutic Strategies and Small-Molecule Modulators in Drug Discovery.Medicinal research reviews · 2026Review
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- Glycolytic enolase 1-induced H4K12 lactylation activates quiescent breast cancer stem-like cells in triple-negative breast cancer.Signal transduction and targeted therapy · 2026Article
- Oncogenic DHX15 mutation enhances mitochondrial metabolism and sustains leukemia stemness.Leukemia · 2026Article
- Shared Major Metabolic Pathways and Potential Targeted Therapies in Malignancies and Systemic Lupus Erythematosus.Biomolecules · 2026Review
- Eucalyptus camaldulensis leaf extract enhances thalidomide efficacy in acute myeloid leukemia cells through modulation of mitochondrial energetics.BMC complementary medicine and therapies · 2026Article
- Myeloid differentiation-associated autophagy drives venetoclax resistance in AML.Research square · 2026Article
798 more citing papers are in PubMed but not listed here.
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14 authors.
Funding
Abstract
Most forms of chemotherapy employ mechanisms involving induction of oxidative stress, a strategy that can be effective due to the elevated oxidative state commonly observed in cancer cells. However, recent studies have shown that relative redox levels in primary tumors can be heterogeneous, suggesting that regimens dependent on differential oxidative state may not be uniformly effective. To investigate this issue in hematological malignancies, we evaluated mechanisms controlling oxidative state in primary specimens derived from acute myelogenous leukemia (AML) patients. Our studies demonstrate three striking findings. First, the majority of functionally defined leukemia stem cells (LSCs) are characterized by relatively low levels of reactive oxygen species (termed "ROS-low"). Second, ROS-low LSCs aberrantly overexpress BCL-2. Third, BCL-2 inhibition reduced oxidative phosphorylation and selectively eradicated quiescent LSCs. Based on these findings, we propose a model wherein the unique physiology of ROS-low LSCs provides an opportunity for selective targeting via disruption of BCL-2-dependent oxidative phosphorylation.
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