Evidence map›Paper›PMID 38262416›Full record

ArticleCell chemical biology2024

PARP trapping is governed by the PARP inhibitor dissociation rate constant.

Angelica A Gopal, Bianca Fernandez, Justin Delano, Ralph Weissleder, J Matthew Dubach

Abstract read
In one paragraph

Article in Cell chemical biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
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  15. Mechanisms of Resistance to PARPi in Pancreatic Ductal Adenocarcinoma.Journal of cellular and molecular medicine · 2025
    Article
  16. BRCA2 reversion mutation-independent resistance to PARP inhibition through impaired DNA prereplication complex function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Review
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

5 authors.

Angelica A GopalInstitute for Innovation in Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.
Bianca FernandezInstitute for Innovation in Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.
Justin DelanoInstitute for Innovation in Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.
Ralph WeisslederCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Department of Systems Biology, Harvard Medical School, Boston, MA 02115.
J Matthew DubachInstitute for Innovation in Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114. Electronic address: dubach.matt@mgh.harvard.edu.

Funding

Optimizing PARP inhibitor therapy through novel approaches to resolve the molecular mechanisms of responseR01CA241179 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DUBACH, JOHN · 2019 to 2023
$1.9M
The role of PARP inhibitor target engagement in breast cancerR00CA198857 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DUBACH, JOHN · 2017 to 2019
$738k
NCI NIH HHS R00 CA198857NCI NIH HHS R01 CA241179
6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) are a class of cancer drugs that enzymatically inhibit PARP activity at sites of DNA damage. Yet, PARPi function mainly by trapping PARP1 onto DNA with a wide range of potency among the clinically relevant inhibitors. How PARPi trap and why some are better trappers remain unknown. Here, we show trapping occurs primarily through a kinetic phenomenon at sites of DNA damage that correlates with PARPi k

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsDNADNA DamageHumansKineticsPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesDNAPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerasesdissociation rateDNA damage repairPARPPARP1PARP inhibitorPARP trappingprotein recruitment

Identifiers

PMID38262416
PMCPMC11259578

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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.