Evidence map›Paper›PMID 25220415›Full record

ReviewOncogene2015

The role of poly(ADP-ribosyl)ation in DNA damage response and cancer chemotherapy.

M Li, X Yu

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Poly-ADP-ribosylation dynamics, signaling, and analysis.Environmental and molecular mutagenesis · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. High Expression ofFrontiers in oncology · 2022
    Article
  11. Review
  12. Article
  13. PARP inhibitor niraparib as a radiosensitizer promotes antitumor immunity of radiotherapy in EGFR-mutated non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  14. Article
  15. Article
  16. ADP-ribosylhydrolases: from DNA damage repair to COVID-19.Journal of Zhejiang University. Science. B · 2021
    Review
  17. Article
  18. Review
  19. Review
  20. Review

3 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

2 authors at 1 institution in 1 country.

M Li1] Department of Obstetrics and Gynecology, Reproductive Medical Center, Peking University Third Hospital, Beijing, China [2] Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
X YuDivision of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

Regulation of Ionizing Radiation-Induced DNA Damage ResponseR01CA130899 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YILUN · 2009 to 2023
$5.5M
Molecular Mechanisms of BRCA1-Dependent DNA Damage Response and TumorogenesisR01CA132755 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHEN, BINGHUI · 2008 to 2019
$3.5M
Functional analysis of BRCA1 in DNA damage response and tumor suppressionR01CA187209 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, XIAOCHUN · 2014 to 2018
$1.7M
Functional analysis of the TET2/OGT complex in epigenetic modificationsR01GM108647 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, XIAOCHUN · 2015 to 2018
$1.3M
NCI NIH HHS CA130899NCI NIH HHS CA132755NCI NIH HHS R01 CA130899NCI NIH HHS R01 CA132755NCI NIH HHS R01 CA187209NIGMS NIH HHS R01 GM108647
6 · The paper itself

Abstract

DNA damage is a deleterious threat, but occurs daily in all types of cells. In response to DNA damage, poly(ADP-ribosyl)ation, a unique post-translational modification, is immediately catalyzed by poly(ADP-ribose) polymerases (PARPs) at DNA lesions, which facilitates DNA damage repair. Recent studies suggest that poly(ADP-ribosyl)ation is one of the first steps of cellular DNA damage response and governs early DNA damage response pathways. Suppression of DNA damage-induced poly(ADP-ribosyl)ation by PARP inhibitors impairs early DNA damage response events. Moreover, PARP inhibitors are emerging as anti-cancer drugs in phase III clinical trials for BRCA-deficient tumors. In this review, we discuss recent findings on poly(ADP-ribosyl)ation in DNA damage response as well as the molecular mechanism by which PARP inhibitors selectively kill tumor cells with BRCA mutations.

Indexed as

AnimalsAntineoplastic AgentsChromatin Assembly and DisassemblyDNA Breaks, Double-StrandedDNA DamageEnzyme InhibitorsHumansNeoplasmsPoly Adenosine Diphosphate RibosePoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProtein Processing, Post-TranslationalTranscription FactorsAntineoplastic AgentsEnzyme InhibitorsPoly Adenosine Diphosphate RibosePoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesTranscription Factors

Identifiers

PMID25220415
PMCPMC4362780
OpenAlexW2077515764

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.