Evidence map›Paper›PMID 24579667›Full record

ReviewCritical reviews in eukaryotic gene expression2014

Review of poly (ADP-ribose) polymerase (PARP) mechanisms of action and rationale for targeting in cancer and other diseases.

Julio Morales, Longshan Li, Farjana J Fattah, Ying Dong, Erik A Bey, Malina Patel, Jinming Gao, David A Boothman

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in eukaryotic gene expression, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 316 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
316citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

316 citing papers in PubMed, 1 synthesis or guideline pooled it, 604 citations in OpenAlex.

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256 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

8 authors at 2 institutions in 1 country.

Julio MoralesSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
Longshan LiSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
Farjana J FattahSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
Ying DongSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
Erik A BeyDepartment of Basic Pharmaceutical Sciences & Mary Bapp Randolph, West Virginia University, Morgantown, WV 26506.
Malina PatelSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
Jinming GaoSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
David A BoothmanSimmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399.
The University of Texas Southwestern Medical Center · USWest Virginia University · US

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Sandi Leigh Pruitt · 2010 to 2026
$53.7M
Use of Beta-Lapachone for Lung Cancer ChemotherapyR01CA102792 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI BOOTHMAN, DAVID A · 2003 to 2017
$5.3M
Ku70 Binding Protein-5 (KUB5), a Novel Factor in Nonhomologous End JoiningR01CA139217 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI BOOTHMAN, DAVID A · 2010 to 2014
$1.7M
NCI NIH HHS P30 CA142543NCI NIH HHS R01 CA102792NCI NIH HHS R01 CA139217
6 · The paper itself

Abstract

Poly (ADP-ribose) polymerases (PARPs) are a family of related enzymes that share the ability to catalyze the transfer of ADP-ribose to target proteins. PARPs play an important role in various cellular processes, including modulation of chromatin structure, transcription, replication, recombination, and DNA repair. The role of PARP proteins in DNA repair is of particular interest, in view of the finding that certain tumors defective in homologous recombination mechanisms, may rely on PARP-mediated DNA repair for survival, and are sensitive to its inhibition. PARP inhibitors may also increase tumor sensitivity to DNA-damaging agents. Clinical trials of PARP inhibitors are investigating the utility of these approaches in cancer. The hyperactivation of PARP has also been shown to result in a specific programmed cell death pathway involving NAD+/ATP depletion, mu-calpain activation, loss of mitochondrial membrane potential, and the release of apoptosis inducing factor. Hyperactivation of the PARP pathway may be exploited to selectively kill cancer cells. Other PARP forms, including tankyrase 1 (PARP 5a), which plays an important role in enhancing telomere elongation by telomerase, have been found to be potential targets in cancer therapy. The PARP pathway and its inhibition thus offers a number of opportunities for therapeutic intervention in both cancer and other disease states.

Indexed as

AnimalsDisease Models, AnimalDNA RepairEnzyme InhibitorsEpigenesis, GeneticHumansMolecular Targeted TherapyNanomedicineNaphthoquinonesNecrosisNeoplasmsPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesTranscription Factorsbeta-lapachoneEnzyme InhibitorsNaphthoquinonesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesTranscription Factors

Identifiers

PMID24579667
PMCPMC4806654
OpenAlexW2151213561

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.