ReviewFrontiers in oncology2023
Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia.
Review in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Engineered flavonoid disrupts mitochondrial AIF/CHCHD4 complex for targeted cancer therapy.Acta pharmaceutica Sinica. B · 2026Article
- Article
- Review
- Multi-omics analysis of pediatric minimally differentiated acute myeloid leukemia reveals RUNX1-driven stemness and chemoresistance.Leukemia · 2026Article
- Suppression of UCP2 alleviates leukemogenesis by enhancing branched-chain amino acids-induced oxidative stress via activating the PI3K/AKT/mTOR signaling pathway.Genes & diseases · 2026Article
- Busulfan resistance in AML is associated with changes in mitochondrial copy number and lipid metabolism.Scientific reports · 2026Article
- Helminth-derived stefin-1 selectively reduces leukemic cell viability and promotes apoptosis in U937 cells.PloS one · 2026Article
- Integrative profiling of lactylation reveals prognostic biomarkers and an immunosuppressive niche in acute myeloid leukemia.Frontiers in immunology · 2026Article
- The ALDH2/PolG2 axis enhances mitochondrial biogenesis via transcriptional regulation of Nrf2 and promotes chemotherapy resistance in acute myeloid leukaemia.Cell death & disease · 2025Article
- Acute myeloid leukemia mitochondria hydrolyze ATP to support oxidative metabolism and resist chemotherapy.Science advances · 2025Article
- STX1A regulates ferroptosis and chemoresistance in gastric cancer through mitochondrial function modulation.Human cell · 2025Article
- The HOX Gene Family's Role as Prognostic and Diagnostic Biomarkers in Hematological and Solid Tumors.Cancers · 2025Review
- Metabolic reprogramming and immune regulation in acute myeloid leukemia.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Chemoresistance often complicates the management of cancer, as noted in the instance of acute myeloid leukemia (AML). Mitochondrial function is considered important for the viability of AML blasts and appears to also modulate chemoresistance. As mitochondrial metabolism is aberrant in AML, any distinct pathways could be directly targeted to impact both cell viability and chemoresistance. Therefore, identifying and targeting those precise rogue elements of mitochondrial metabolism could be a valid therapeutic strategy in leukemia. Here, we review the evidence for abnormalities in mitochondria metabolic processes in AML cells, that likely impact chemoresistance. We further address several therapeutic approaches targeting isocitrate dehydrogenase 2 (IDH2), CD39, nicotinamide phosphoribosyl transferase (NAMPT), electron transport chain (ETC) complex in AML and also consider the roles of mesenchymal stromal cells. We propose the term "mitotherapy" to collectively refer to such regimens that attempt to override mitochondria-mediated metabolic reprogramming, as used by cancer cells. Mounting evidence suggests that mitotherapy could provide a complementary strategy to overcome chemoresistance in liquid cancers, as well as in solid tumors.
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