Evidence map›Paper›PMID 30538273›Full record

ReviewNature reviews. Cancer2019

Post-GWAS in prostate cancer: from genetic association to biological contribution.

Samaneh Farashi, Thomas Kryza, Judith Clements, Jyotsna Batra

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
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  10. Review
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  13. piRNA PROPER Suppresses DUSP1 Translation by Targeting NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Advances in Prostate Cancer Biomarkers and Probes.Cyborg and bionic systems (Washington, D.C.) · 2024
    Review
  18. Article
  19. Review
  20. Review

4 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

4 authors at 1 institution in 1 country.

Samaneh FarashiCancer Program, School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.
Thomas KryzaCancer Program, School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.
Judith ClementsCancer Program, School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.
Jyotsna BatraCancer Program, School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia. jyotsna.batra@qut.edu.au.ORCID http://orcid.org/0000-0003-4646-6247
Translational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have been successful in deciphering the genetic component of predisposition to many human complex diseases including prostate cancer. Germline variants identified by GWAS progressively unravelled the substantial knowledge gap concerning prostate cancer heritability. With the beginning of the post-GWAS era, more and more studies reveal that, in addition to their value as risk markers, germline variants can exert active roles in prostate oncogenesis. Consequently, current research efforts focus on exploring the biological mechanisms underlying specific susceptibility loci known as causal variants by applying novel and precise analytical methods to available GWAS data. Results obtained from these post-GWAS analyses have highlighted the potential of exploiting prostate cancer risk-associated germline variants to identify new gene networks and signalling pathways involved in prostate tumorigenesis. In this Review, we describe the molecular basis of several important prostate cancer-causal variants with an emphasis on using post-GWAS analysis to gain insight into cancer aetiology. In addition to discussing the current status of post-GWAS studies, we also summarize the main molecular mechanisms of potential causal variants at prostate cancer risk loci and explore the major challenges in moving from association to functional studies and their implication in clinical translation.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansMaleProstatic NeoplasmsSignal Transduction

Identifiers

PMID30538273
OpenAlexW2904868717

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.