ReviewCurrent drug metabolism2015
Role of Drug Metabolism in the Cytotoxicity and Clinical Efficacy of Anthracyclines.
Review in Current drug metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Meta analysis of bioactive compounds, miRNA, siRNA and cell death regulators as sensitizers to doxorubicin induced chemoresistance.Apoptosis : an international journal on programmed cell death · 2022Pooled it
- Potential Mechanisms of MAP Kinase JNK's Involvement in Modulating Cancer Cell Fate in a Cisplatin Concentration-Dependent Manner.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Microbiome dysbiosis and chemotherapy resistance in acute myeloid leukemia (AML).NPJ biofilms and microbiomes · 2025Review
- Heterogeneity in Cancer.Cancers · 2025Review
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- Article
- Enhancement of antitumor effects of berberine chloride with a copper(II) complex against human triple negative breast cancer:Results in chemistry · 2024Article
- Integrated drug resistance and leukemic stemness gene-expression scores predict outcomes in large cohort of over 3500 AML patients from 10 trials.NPJ precision oncology · 2024Article
- Circumvention of Topoisomerase IIMolecular pharmacology · 2024Article
- Use of CRISPR/Cas9 with Homology-Directed Repair to Gene-Edit Topoisomerase IIThe Journal of pharmacology and experimental therapeutics · 2024Article
- Quantitative imaging of doxorubicin diffusion and cellular uptake in biomimetic gels with human liver tumor cells.Drug delivery and translational research · 2024Article
- The Temozolomide-Doxorubicin paradox in Glioblastoma in vitro-in silico preclinical drug-screening.Scientific reports · 2024Article
- A review of chemotherapeutic drugs-induced arrhythmia and potential intervention with traditional Chinese medicines.Frontiers in pharmacology · 2024Review
- Molecular assessment of drug-phospholipid interactions consequent to cancer treatment: a study of anthracycline-induced cardiotoxicity.Scientific reports · 2023Article
- Differences in susceptibility to ADR nephropathy among C57BL/6 substrains.Experimental animals · 2023Article
- The Role of Natural Products in the Improvement of Cancer-Associated Cachexia.International journal of molecular sciences · 2023Review
- Effects of hsa-miR-9-3p and hsa-miR-9-5p on Topoisomerase IIThe Journal of pharmacology and experimental therapeutics · 2023Article
- Concomitant delivery of doxorubicin and cisplatin through liposome-based thermosensitive nanoparticles: perspective in the treatment of cancer in animal models.American journal of cancer research · 2023Article
- Article
- Biocompatible, Multi-Mode, Fluorescent,Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many clinical studies involving anti-tumor agents neglect to consider how these agents are metabolized within the host and whether the creation of specific metabolites alters drug therapeutic properties or toxic side effects. However, this is not the case for the anthracycline class of chemotherapy drugs. This review describes the various enzymes involved in the one electron (semi-quinone) or two electron (hydroxylation) reduction of anthracyclines, or in their reductive deglycosidation into deoxyaglycones. The effects of these reductions on drug antitumor efficacy and toxic side effects are also discussed. Current evidence suggests that the one electron reduction of anthracyclines augments both their tumor toxicity and their toxicity towards the host, in particular their cardiotoxicity. In contrast, the two electron reduction (hydroxylation) of anthracyclines strongly reduces their ability to kill tumor cells, while augmenting cardiotoxicity through their accumulation within cardiomyocytes and their direct effects on excitation/contraction coupling within the myocytes. The reductive deglycosidation of anthracyclines appears to inactivate the drug and only occurs under rare, anaerobic conditions. This knowledge has resulted in the identification of important new approaches to improve the therapeutic index of anthracyclines, in particular by inhibiting their cardiotoxicity. The true utility of these approaches in the management of cancer patients undergoing anthracycline-based chemotherapy remains unclear, although one such agent (the iron chelator dexrazoxane) has recently been approved for clinical use.
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