ArticleOncotarget2010
Homologous recombination repair is essential for repair of vosaroxin-induced DNA double-strand breaks.
Article in Oncotarget, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- REVEAL-1, a phase 2 dose regimen optimization study of vosaroxin in older poor-risk patients with previously untreated acute myeloid leukaemia.British journal of haematology · 2015Trial
- Antiproliferative Activities of Lipophililic Fluoroquinolones- Based Scaffold Against a Panel of Solid and Liquid Cancer Cell Lines.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- The benzylisoquinoline alkaloids, berberine and coptisine, act against camptothecin-resistant topoisomerase I mutants.Scientific reports · 2021Article
- Early changes in rpS6 phosphorylation and BH3 profiling predict response to chemotherapy in AML cells.PloS one · 2018Article
- Metabolism and disposition of the anticancer quinolone derivative vosaroxin, a novel inhibitor of topoisomerase II.Investigational new drugs · 2017Article
- Enhancement of radiosensitivity by the novel anticancer quinolone derivative vosaroxin in preclinical glioblastoma models.Oncotarget · 2017Article
- Targeting acute myeloid leukemia with TP53-independent vosaroxin.Future oncology (London, England) · 2017Review
- Therapies for acute myeloid leukemia: vosaroxin.OncoTargets and therapy · 2017Review
- Review
- Article
- Dynamics of double strand breaks and chromosomal translocations.Molecular cancer · 2014Review
- A DNA repair pathway score predicts survival in human multiple myeloma: the potential for therapeutic strategy.Oncotarget · 2014Article
- A Small-Molecule Inhibitor of RAD51 Reduces Homologous Recombination and Sensitizes Multiple Myeloma Cells to Doxorubicin.Frontiers in oncology · 2014Article
- Evaluation of candidate biomarkers to predict cancer cell sensitivity or resistance to PARP-1 inhibitor treatment.Cell cycle (Georgetown, Tex.) · 2012Article
- BRCA1-directed, enhanced and aberrant homologous recombination: mechanism and potential treatment strategies.Cell cycle (Georgetown, Tex.) · 2012Review
- Poly(ADP-ribose) polymerase inhibition enhances p53-dependent and -independent DNA damage responses induced by DNA damaging agent.Cell cycle (Georgetown, Tex.) · 2011Article
- Recent progress in targeting cancer.Aging · 2011Review
- Do AML patients with DNMT3A exon 23 mutations benefit from idarubicin as compared to daunorubicin? A single center experience.Oncotarget · 2011Article
- Effects of conditional depletion of topoisomerase II on cell cycle progression in mammalian cells.Cell cycle (Georgetown, Tex.) · 2011Article
- Pleiotropic functions of EAPII/TTRAP/TDP2: cancer development, chemoresistance and beyond.Cell cycle (Georgetown, Tex.) · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Vosaroxin (formerly voreloxin) is a first-in-class anticancer quinolone derivative that intercalates DNA and inhibits topoisomerase II, inducing site-selective double-strand breaks (DSB), G2 arrest and apoptosis. Objective responses and complete remissions were observed in phase 2 studies of vosaroxin in patients with solid and hematologic malignancies, and responses were seen in patients whose cancers were resistant to anthracyclines. The quinolone-based scaffold differentiates vosaroxin from the anthracyclines and anthracenediones, broadly used DNA intercalating topoisomerase II poisons. Here we report that vosaroxin induces a cell cycle specific pattern of DNA damage and repair that is distinct from the anthracycline, doxorubicin. Both drugs stall replication and preferentially induce DNA damage in replicating cells, with damage in G2 / M > S >> G1. However, detectable replication fork collapse, as evidenced by DNA fragmentation and long tract recombination during S phase, is induced only by doxorubicin. Furthermore, vosaroxin induces less overall DNA fragmentation. Homologous recombination repair (HRR) is critical for recovery from DNA damage induced by both agents, identifying the potential to clinically exploit synthetic lethality.
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What OpenQuestion holds
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 OpenQuestion graph.