Evidence map›Paper›PMID 20823146›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2010

Histone gammaH2AX and poly(ADP-ribose) as clinical pharmacodynamic biomarkers.

Christophe E Redon, Asako J Nakamura, Yong-Wei Zhang, Jiuping Jay Ji, William M Bonner, Robert J Kinders, Ralph E Parchment, James H Doroshow, Yves Pommier

Open access · bronzeAbstract readEvaluation StudyReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

140 citing papers in PubMed, 256 citations in OpenAlex.

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  6. PARP1 deficiency mitigates amyloid pathology, neurodegeneration, and cognitive decline in a familial Alzheimer's disease model.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  8. DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025
    Review
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80 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

9 authors at 2 institutions in 1 country.

Christophe E RedonLaboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Asako J Nakamura
Yong-Wei Zhang
Jiuping Jay Ji
William M Bonner
Robert J Kinders
Ralph E Parchment
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
Phase 01 Clinical TrialsZIABC011078 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DOROSHOW, JAMES · 2009 to 2025
$9.0M
Studies of Histone Functions in Chromatin; H2AX and DNA DSBsZIABC006140 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BONNER, WILLIAM · 2009 to 2015
$7.8M
PROTEIN-ASSOCIATED DNA BREAKS AS INDICATOR OF TOPOISOMERASE INHIBITIONZ01BC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 1996 to 2008
$1.5M
Intramural NIH HHS Z01 BC006150
6 · The paper itself

Abstract

Tumor cells are often deficient in DNA damage response (DDR) pathways, and anticancer therapies are commonly based on genotoxic treatments using radiation and/or drugs that damage DNA directly or interfere with DNA metabolism, leading to the formation of DNA double-strand breaks (DSB), and ultimately to cell death. Because DSBs induce the phosphorylation of histone H2AX (γH2AX) in the chromatin flanking the break site, an antibody directed against γH2AX can be employed to measure DNA damage levels before and after patient treatment. Poly(ADP-ribose) polymerases (PARP1 and PARP2) are also activated by DNA damage, and PARP inhibitors show promising activity in cancers with defective homologous recombination (HR) pathways for DSB repair. Ongoing clinical trials are testing combinations of PARP inhibitors with DNA damaging agents. Poly(ADP-ribosylation), abbreviated as PAR, can be measured in clinical samples and used to determine the efficiency of PARP inhibitors. This review summarizes the roles of γH2AX and PAR in the DDR, and their use as biomarkers to monitor drug response and guide clinical trials, especially phase 0 clinical trials. We also discuss the choices of relevant samples for γH2AX and PAR analyses.

Indexed as

Biomarkers, PharmacologicalAnimalsAntineoplastic AgentsBiomarkers, TumorDNA DamageHistonesHumansMedical OncologyModels, BiologicalNeoplasmsPoly Adenosine Diphosphate RibosePoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesPrognosisAntineoplastic AgentsBiomarkers, PharmacologicalBiomarkers, TumorH2AX protein, humanHistonesPoly Adenosine Diphosphate RibosePoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerases

Identifiers

PMID20823146
PMCPMC2940983
OpenAlexW2145676287

What OpenQuestion holds

Textmetadata
LicenceTDM
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.