Evidence map›Paper›PMID 33044685›Full record

ReviewTargeted oncology2020

Poly(ADP-Ribose) Polymerase Inhibitors in Prostate Cancer: Molecular Mechanisms, and Preclinical and Clinical Data.

Dawid Sigorski, Ewa Iżycka-Świeszewska, Lubomir Bodnar

Open access · hybridAbstract readReview
In one paragraph

Review in Targeted oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. PathogenicCancers · 2021
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Prognostic Value ofBiomedicines · 2020
    Article
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

3 authors at 3 institutions in 2 countries.

Dawid SigorskiDepartment of Oncology, Collegium Medicum, University of Warmia and Mazury, Al. Wojska Polskiego 37, 10-228, Olsztyn, Poland. dawidsigorski@wp.pl.ORCID http://orcid.org/0000-0002-4799-9611
Ewa Iżycka-ŚwieszewskaDepartment of Pathology and Neuropathology, Medical University of Gdańsk, Gdańsk, Poland.ORCID http://orcid.org/0000-0001-7550-1326
Lubomir BodnarDepartment of Oncology, Collegium Medicum, University of Warmia and Mazury, Al. Wojska Polskiego 37, 10-228, Olsztyn, Poland.ORCID http://orcid.org/0000-0001-8548-8778
Gdańsk Medical University · PLMinisterio del Interior · ESUniversity of Warmia and Mazury in Olsztyn · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability is one of the hallmarks of cancer. The incidence of genetic alterations in homologous recombination repair genes increases during cancer progression, and 20% of prostate cancers (PCas) have defects in DNA repair genes. Several somatic and germline gene alterations drive prostate cancer tumorigenesis, and the most important of these are BRCA2, BRCA1, ATM and CHEK2. There is a group of BRCAness tumours that share phenotypic and genotypic properties with classical BRCA-mutated tumours. Poly(ADP-ribose) polymerase inhibitors (PARPis) show synthetic lethality in cancer cells with impaired homologous recombination genes, and patients with these alterations are candidates for PARPi therapy. Androgen deprivation therapy is the mainstay of PCa therapy. PARPis decrease androgen signalling by interaction with molecular mechanisms of the androgen nuclear complex. The PROFOUND phase III trial, comparing olaparib with enzalutamide/abiraterone therapy, revealed increased radiological progression-free survival (rPFS) and overall survival (OS) among patients with metastatic castration-resistant prostate cancer (mCRPC) with BRCA1, BRCA2 or ATM mutations. The clinical efficacy of PARPis has been confirmed in ovarian, breast, pancreatic and recently also in a subset of PCa. There is growing evidence that molecular tumour boards are the future of the oncological therapeutic approach in prostate cancer. In this review, we summarise the data concerning the molecular mechanisms and preclinical and clinical data of PARPis in PCa.

Indexed as

Genetic TestingHumansMalePoly(ADP-ribose) Polymerase InhibitorsProstatic Neoplasms, Castration-ResistantPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID33044685
PMCPMC7701127
OpenAlexW3092221049

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.