Evidence map›Paper›PMID 32790034›Full record

ReviewThe oncologist2021

PARP Inhibitors and Prostate Cancer: To Infinity and Beyond BRCA.

Emily N Risdon, Cindy H Chau, Douglas K Price, Oliver Sartor, William D Figg

Open access · bronzeAbstract readReview
In one paragraph

Review in The oncologist, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.1field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

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7 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

5 authors at 3 institutions in 1 country.

Emily N RisdonGenitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Cindy H ChauGenitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Douglas K PriceGenitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Oliver SartorTulane Medical School, New Orleans, Louisiana, USA.ORCID 0000-0002-8777-7343
William D FiggGenitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.ORCID 0000-0003-2428-5613
Center for Cancer Research · USNational Cancer Institute · USTulane Medical Center · US

Funding

Identify SNPs and Polymorphisms Involved in the Development of Prostate CancerZIABC010453 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2009 to 2025
$10.4M
Drug Development for Prostate Cancer and other Metastatic ProcessesZIABC010547 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2009 to 2025
$10.2M
Intramural NIH HHS ZIA BC010547
6 · The paper itself

Abstract

The U.S. Food and Drug Administration recently approved two poly-adenosine diphosphate-ribose polymerase (PARP) inhibitors, olaparib and rucaparib, for treatment of biomarker-positive metastatic castrate resistant prostate cancer. The benefits of PARP inhibition have been well characterized in patients who have BRCA1 and BRCA2 mutations in several forms of cancer. BRCA1 and BRCA2 occupy key roles in DNA damage repair, which is comprised of several different pathways with numerous participants. Patients with mutations in other key genes within the DNA damage repair pathway may also respond to treatment with PARP inhibitors, and identification of these alterations could significantly increase the percentage of patients that may benefit from PARP inhibition. This review focuses on the potential for synthetically lethal interactions between PARP inhibitors and non-BRCA DNA damage repair genes. IMPLICATIONS FOR PRACTICE: The treatment potential of PARP inhibition has been well characterized in patients with BRCA1 and BRCA2 mutations, but there is compelling evidence for expanding the use of PARP inhibitors to mutations of other non-BRCA DNA damage repair (DDR) genes. This could increase the percentage of patients that may benefit from treatment with PARP inhibitors alone or in combination with other therapies. Understanding the significance of PARP inhibitor-sensitizing alterations in other common non-BRCA DDR genes will help guide clinical decisions to provide targeted treatment options to a wider population of patients.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsProstatic NeoplasmsBRCA1 ProteinBRCA2 ProteinDNA RepairGenes, BRCA2HumansMalePoly(ADP-ribose) PolymerasesBRCA1 ProteinBRCA2 ProteinPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesBiomarkerBRCADNA damage repairHomologous recombination repairMismatch repairMutationOlaparibPoly(ADP-ribose) polymerase inhibitorProstate cancerRucaparib

Identifiers

PMID32790034
PMCPMC7794174
OpenAlexW3048583805

What OpenQuestion holds

Textmetadata
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.