Evidence map›Paper›PMID 26091341›Full record

ArticleMolecular cell2015

Chromatin to Clinic: The Molecular Rationale for PARP1 Inhibitor Function.

Felix Y Feng, Johann S de Bono, Mark A Rubin, Karen E Knudsen

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
10.5field-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

81 citing papers in PubMed, 136 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Protein Acetylation and NAD+ Homeostasis in Aging Muscle.Advances in experimental medicine and biology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Olaparib Attenuates Demyelination and Neuroinflammation in an Organotypic Slice Culture Model of Metachromatic Leukodystrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. The lactate-NADCell reports · 2022
    Article
  15. Review
  16. Review
  17. Article
  18. Cancer research · 2021
    Article
  19. Article
  20. Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.International journal of molecular sciences · 2021
    Review

21 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

4 authors at 4 institutions in 2 countries.

Felix Y FengMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, 48109, USA; Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, 48109, USA.
Johann S de BonoProstate Cancer Targeted Therapy Group, The Royal Marsden NHS Foundation Trust, Downs Road, Sutton, Surrey SM2 5PT, UK.
Mark A RubinInstitute for Precision Medicine of Weill Cornell Medical College and NewYork-Presbyterian Hospital; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College; Department of Urology, Weill Cornell Medical College; Meyer Cancer Center of Weill Cornell Medical College and New York-Presbyterian Hospital, New York, NY 10021, USA.
Karen E KnudsenDepartment of Cancer Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA; Department of Urology, Thomas Jefferson University, Philadelphia, PA 19107, USA; Department of Radiation Oncology, Thomas Jefferson University, Philadelphia, PA 19107, USA; Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: karen.knudsen@jefferson.edu.
NewYork–Presbyterian Hospital · USRoyal Marsden NHS Foundation Trust · GBSidney Kimmel Cancer Center · USUniversity of Michigan–Ann Arbor · US

Funding

Cyclin D1: repercussions of AR control and alternative splicing in prostate canceR01CA099996 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2003 to 2013
$2.6M
NCI NIH HHS R01 CA099996
6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors were recently shown to have potential clinical impact in a number of disease settings, particularly as related to cancer therapy, treatment for cardiovascular dysfunction, and suppression of inflammation. The molecular basis for PARP1 inhibitor function is complex, and appears to depend on the dual roles of PARP1 in DNA damage repair and transcriptional regulation. Here, the mechanisms by which PARP-1 inhibitors elicit clinical response are discussed, and strategies for translating the preclinical elucidation of PARP-1 function into advances in disease management are reviewed.

Indexed as

DNA RepairTranscription, GeneticChromatinEnzyme InhibitorsHumansMolecular Targeted TherapyNeoplasmsPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesTranslational Research, BiomedicalChromatinEnzyme InhibitorsPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerases

Identifiers

PMID26091341
PMCPMC4487541
OpenAlexW1842469464

What OpenQuestion holds

Textmetadata
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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.