Evidence map›Paper›PMID 31357527›Full record

ReviewGenes2019

PARP Inhibitors in Prostate Cancer—The Preclinical Rationale and Current Clinical Development.

Verneri Virtanen, Kreetta Paunu, Johanna K Ahlskog, Reka Varnai, Csilla Sipeky, Maria Sundvall

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.9field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
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  16. AR and PI3K/AKT in Prostate Cancer: A Tale of Two Interconnected Pathways.International journal of molecular sciences · 2023
    Review
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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

6 authors at 3 institutions in 2 countries.

Verneri VirtanenInstitute of Biomedicine, and Cancer Research Laboratories, Western Cancer Centre FICAN West,University of Turku, FI-20520 Turku, Finland.
Kreetta PaunuInstitute of Biomedicine, and Cancer Research Laboratories, Western Cancer Centre FICAN West,University of Turku, FI-20520 Turku, Finland.
Johanna K AhlskogFaculty of Science and Engineering, Åbo Akademi University, and Turku Bioscience,University of Turku and Åbo Akademi University, FI-20520 Turku, Finland.
Reka VarnaiDepartment of Primary Health Care, University of Pécs, H-7623 Pécs, Hungary.
Csilla SipekyInstitute of Biomedicine, University of Turku, FI-20520 Turku, Finland.
Maria SundvallInstitute of Biomedicine, and Cancer Research Laboratories, Western Cancer Centre FICAN West,University of Turku, FI-20520 Turku, Finland. maria.sundvall@utu.fi.
University of Turku · FIÅbo Akademi University · FIUniversity of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is globally the second most commonly diagnosed cancer type in men. Recent studies suggest that mutations in DNA repair genes are associated with aggressive forms of prostate cancer and castration resistance. Prostate cancer with DNA repair defects may be vulnerable to therapeutic targeting by Poly(ADP-ribose) polymerase (PARP) inhibitors. PARP enzymes modify target proteins with ADP-ribose in a process called PARylation and are in particular involved in single strand break repair. The rationale behind the clinical trials that led to the current use of PARP inhibitors to treat cancer was to target the dependence of BRCA-mutant cancer cells on the PARP-associated repair pathway due to deficiency in homologous recombination. However, recent studies have proposed therapeutic potential for PARP inhibitors in tumors with a variety of vulnerabilities generating dependence on PARP beyond the synthetic lethal targeting of BRCA1/BRCA2 mutated tumors, suggesting a wider potential than initially thought. Importantly, PARP-associated DNA repair pathways are also closely connected to androgen receptor (AR) signaling, which is a key regulator of tumor growth and a central therapeutic target in prostate cancer. In this review, we provide an extensive overview of published and ongoing trials exploring PARP inhibitors in treatment of prostate cancer and discuss the underlying biology. Several clinical trials are currently studying PARP inhibitor mono- and combination therapies in the treatment of prostate cancer. Integration of drugs targeting DNA repair pathways in prostate cancer treatment modalities allows developing of more personalized care taking also into account the genetic makeup of individual tumors.

Indexed as

AnimalsAntineoplastic AgentsClinical Trials as TopicDrug Evaluation, PreclinicalHumansMalePoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProstatic NeoplasmsAntineoplastic AgentsPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerasescastration resistant prostate cancerDNA damage repairPARP inhibitorsprecision medicine

Identifiers

PMID31357527
PMCPMC6723995
OpenAlexW2965457822

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.