ArticleCancer discovery2024
Targeting Acute Myeloid Leukemia Stem Cells through Perturbation of Mitochondrial Calcium.
Article in Cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Mitochondrial transfer in acute myeloid leukaemia and multiple myeloma: Mechanisms, consequences and potential therapeutic opportunities.The FEBS journal · 2026Review
- Bone marrow stromal cells promote chemoresistance in acute myeloid leukaemia through P2RX7-mediated antioxidant defence.Experimental & molecular medicine · 2026Article
- Fatty acid oxidation fuels mitochondrial respiration to drive epidermal stem cell fate and differentiation.Nature communications · 2026Article
- Redox Homeostasis, Metabolic Pathways and Plasticity in Uveal Melanoma Compared to Other Cancers.Cancers · 2026Review
- MO-IPS suppresses acute myeloid leukemia through metabolic reprogramming and synergizes with anti-PD-1 immunotherapy.Functional & integrative genomics · 2026Article
- Diving into the transcriptional landscape of leukemic stem cells in acute myeloid leukemia at single-cell resolution.Journal of cancer research and clinical oncology · 2026Review
- Targeting mitochondrial calcium homeostasis via novel S100A9 inhibitor B2 as a promising agent against AML.Journal of translational medicine · 2026Article
- Bispecific CD37-Siglec6 CAR‑T cells exhibit enhanced anti‑leukemic activity and reduced exhaustion in acute myeloid leukemia xenograft models.Journal of translational medicine · 2026Article
- Effects and molecular mechanism of inhibiting p53 signaling pathway by NSUN4 on the resistance to BCL-2 inhibitor for diffuse large B-cell lymphoma.Clinical and experimental medicine · 2026Article
- The STAT3-VDAC1 axis modulates mitochondrial function and plays a critical role in the survival of acute myeloid leukemia cells.Haematologica · 2026Article
- DRESIS 2.0: the comprehensive landscape of drug resistance information.Nucleic acids research · 2026Article
- Regulating Ferroptosis in Leukemic Stem Cells: From Stemness Preservation to Targeted Differentiation Strategies.Stem cell reviews and reports · 2026Review
- Mitochondria: from powerhouses of cells to hubs in antitumor immunity.Frontiers in immunology · 2026Review
- Multi-omics classification of acute myeloid leukemia guides drug combinations to overcome Venetoclax resistance.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- Pim1 Serves as a Therapeutic Target for Inflammatory Arthritis via Mitochondrial Metabolism and Th17 Cell Differentiation.Research (Washington, D.C.) · 2026Article
- Liposomal mitoxantrone, venetoclax and azacitidine in relapsed/refractory acute myeloid leukaemia and early induction failure: a single-centre real-world study.Frontiers in oncology · 2026Article
- Nonionotropic action of an acid-sensing ion channel inhibits leukemogenesis in the acidic bone marrow niche.The Journal of clinical investigation · 2025Article
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- A novel strategy to target metabolic dependencies in acute myeloid leukemia.Cell death & disease · 2025Article
- siRNA Mediated Genetic Perturbation of Primary Human Leukemia Stem and Progenitor Cells.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
24 authors.
Funding
Abstract
Acute myeloid leukemia stem cells (LSCs) are uniquely reliant on oxidative phosphorylation (OXPHOS) for survival. Moreover, maintenance of OXPHOS is dependent on BCL-2, creating a therapeutic opportunity to target LSCs using the BCL-2 inhibitor venetoclax. Although venetoclax-based regimens have shown promising clinical activity, the emergence of drug resistance is prevalent. Thus, in the present study, we investigated how mitochondrial properties may influence venetoclax responsiveness. Our data show that utilization of mitochondrial calcium is fundamentally different between drug-responsive and nonresponsive LSCs. By comparison, venetoclax-resistant LSCs demonstrate an active metabolic (i.e., OXPHOS) status with relatively high levels of calcium. Consequently, we tested genetic and pharmacological approaches to target the mitochondrial calcium uniporter. We demonstrate that inhibition of calcium uptake reduces OXPHOS and leads to eradication of venetoclax-resistant LSCs. These findings demonstrate a central role for calcium signaling in LSCs and provide an avenue for clinical management of venetoclax resistance. Significance: We identify increased utilization of mitochondrial calcium as a distinct metabolic requirement of venetoclax-resistant LSCs and demonstrate the potential of targeting mitochondrial calcium uptake as a therapeutic strategy.
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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 Socratic graph.