Evidence map›Paper›PMID 21227924›Full record

ArticleNucleic acids research2011

Poly(ADP-ribose) polymerase and XPF-ERCC1 participate in distinct pathways for the repair of topoisomerase I-induced DNA damage in mammalian cells.

Yong-Wei Zhang, Marie Regairaz, Jennifer A Seiler, Keli K Agama, James H Doroshow, Yves Pommier

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

97 citing papers in PubMed, 156 citations in OpenAlex.

  1. Trial
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  6. The Mode of Action and Clinical Outcomes of Sacituzumab Govitecan in Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Review
  7. Review
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  11. Review
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  15. New Life of Topoisomerase I Inhibitors as Antibody-Drug Conjugate Warheads.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yong-Wei ZhangLaboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.
Marie Regairaz
Jennifer A Seiler
Keli K Agama
James H Doroshow
Yves Pommier
Center for Cancer Research · USNational Cancer Institute · US

Funding

DNA Repair, Cell Cycle Checkpoints and Apoptosis as Targets for Anticancer DrugsZIABC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$23.0M
DNA Topoisomerases as Target of Action of Anticancer DrugsZIABC006161 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$16.8M
Phase 01 Clinical TrialsZIABC011078 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DOROSHOW, JAMES · 2009 to 2025
$9.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Poly(ADP-Ribose) (PAR) polymerase (PARP) inhibitors represent a promising class of novel anticancer agents. The present study explores the molecular rationale for combining veliparib (ABT-888) with camptothecin (CPT) and its clinical derivatives, topotecan and irinotecan. ABT-888 inhibited PAR induction by CPT and increased CPT-induced cell killing and histone γH2AX. Increased DNA breaks by ABT-888 were not associated with a corresponding increase of topoisomerase I cleavage complexes and were further increased by inactivation of tyrosyl-DNA phosphodiesterase 1. SiRNA knockdown for the endonuclease XPF-ERCC1 reduced the ABT-888-induced γH2AX response in non-replicating and replicating cells but enhanced the antiproliferative effect of ABT-888 in CPT-treated cells. Our findings indicate the involvement of XPF-ERCC1 in inducing γH2AX response and repairing topoisomerase I-induced DNA damage as an alternative pathway from PARP and tyrosyl-DNA phosphodiesterase 1.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsAntineoplastic Combined Chemotherapy ProtocolsBenzimidazolesCamptothecinCell Line, TumorDNA-Binding ProteinsDNA DamageDNA RepairDNA ReplicationDNA Topoisomerases, Type IEndonucleasesEnzyme InhibitorsHistonesHumansPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsBenzimidazolesCamptothecinDNA-Binding ProteinsDNA Topoisomerases, Type IEndonucleasesEnzyme InhibitorsERCC1 protein, humanH2AX protein, humanHistonesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesTopoisomerase I Inhibitorsveliparibxeroderma pigmentosum group F protein

Identifiers

PMID21227924
PMCPMC3089458
OpenAlexW2030586091

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.