ArticleCancer2016
Impaired mitochondrial function is abrogated by dexrazoxane in doxorubicin-treated childhood acute lymphoblastic leukemia survivors.
Article in Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Trial
- Fatigue among adult survivors of childhood cancer: findings from the French Childhood Cancer Survivor Study.Journal of cancer survivorship : research and practice · 2026Article
- Anthracyclines effect on mitochondrial function and biogenesis in normal blood cells of hodgkin lymphoma patients.Scientific reports · 2025Article
- Mutational analysis of the mitochondrial tRNA genes and flanking regions in lymphocytes from long-term pediatric cancer survivors given doxorubicin chemotherapy for acute lymphoblastic leukemia.Cardio-oncology (London, England) · 2025Article
- Safety of cardiorespiratory and muscle fitness assessment in two children with leukemia during early chemotherapy.Journal of pediatric rehabilitation medicine · 2025Article
- Pharmacotherapy for Cancer Treatment-Related Cardiac Dysfunction and Heart Failure in Childhood Cancer Survivors.Paediatric drugs · 2023Review
- Premature aging in childhood cancer survivors.Oncology letters · 2023Review
- Protective Effects ofMolecules (Basel, Switzerland) · 2022Article
- Promising anti-leukemic effect of Zataria multiflora extract in combination with doxorubicin to combat acute lymphoblastic leukemia cells (Nalm-6) (in vitro and in silico).Scientific reports · 2022Article
- Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management.Journal of hematology & oncology · 2022Review
- The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside.Oxidative medicine and cellular longevity · 2022Review
- Biomarkers of cardiometabolic complications in survivors of childhood acute lymphoblastic leukemia.Scientific reports · 2020Article
- Frailty and aging in cancer survivors.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Rethinking COVID-19 in children: Lessons learned from pediatric viral and inflammatory cardiovascular diseases.Progress in pediatric cardiology · 2020Article
- From old to new - Repurposing drugs to target mitochondrial energy metabolism in cancer.Seminars in cell & developmental biology · 2020Review
- Mechanisms of Anthracycline-Induced Cardiotoxicity: Is Mitochondrial Dysfunction the Answer?Frontiers in cardiovascular medicine · 2020Review
- Strategies to prevent anthracycline-induced cardiotoxicity in cancer survivors.Cardio-oncology (London, England) · 2019Review
- Effects of dexrazoxane on doxorubicin-related cardiotoxicity and second malignant neoplasms in children with osteosarcoma: a report from the Children's Oncology Group.Cardio-oncology (London, England) · 2019Article
- Anthracycline cardiotoxicity: the importance of horizontally integrating pre-clinical and clinical research.Cardiovascular research · 2018Article
- The cardioprotective effect of dexrazoxane (Cardioxane) is consistent with sequestration of poly(ADP-ribose) by self-assembly and not depletion of topoisomerase 2B.Ecancermedicalscience · 2018Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundImpaired cardiac function in doxorubicin-treated childhood cancer survivors is partly mediated by the disruption of mitochondrial energy production. Doxorubicin intercalates into mitochondrial DNA (mtDNA) and disrupts genes encoding for polypeptides that make adenosine triphosphate.
methodsThis cross-sectional study examined mtDNA copy numbers per cell and oxidative phosphorylation (OXPHOS) in peripheral blood mononuclear cells (PBMCs) in 64 childhood survivors of high-risk acute lymphoblastic leukemia (ALL) who had been treated on Dana-Farber Cancer Institute childhood ALL protocols and had received doxorubicin alone (42%) or doxorubicin with the cardioprotectant dexrazoxane (58%). The number of mtDNA copies per cell and the OXPHOS enzyme activity of nicotinamide adenine dinucleotide dehydrogenase (complex I [CI]) and cytochrome c oxidase (complex IV [CIV]) were measured with quantitative real-time polymerase chain reaction immunoassays and thin-layer chromatography, respectively.
resultsAt a median follow-up of 7.8 years after treatment, the median number of mtDNA copies per cell for patients treated with doxorubicin alone (1106.3) was significantly higher than the median number for those who had also received dexrazoxane (310.5; P = .001). No significant differences were detected between the groups for CI or CIV activity.
conclusionsDoxorubicin-treated survivors had an increased number of PBMC mtDNA copies per cell, and concomitant use of dexrazoxane was associated with a lower number of mtDNA copies per cell. Because of a possible compensatory increase in mtDNA copies per cell to maintain mitochondrial function in the setting of mitochondrial dysfunction, overall OXPHOS activity was not different between the groups. The long-term sustainability of this compensatory response in these survivors at risk for cardiac dysfunction over their lifespan is concerning.
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