Evidence map›Paper›PMID 30808988›Full record

ReviewNature reviews. Urology2019

The influence of BRCA2 mutation on localized prostate cancer.

Renea A Taylor, Michael Fraser, Richard J Rebello, Paul C Boutros, Declan G Murphy, Robert G Bristow, Gail P Risbridger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Urology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
6.8field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  3. Observational
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  19. Article
  20. Complexities of Prostate Cancer.International journal of molecular sciences · 2022
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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

7 authors at 5 institutions in 4 countries.

Renea A TaylorMonash Partners Comprehensive Cancer Consortium and Cancer Program, Biomedicine Discovery Institute, Prostate Cancer Research Group, Department of Anatomy and Developmental Biology and Department of Physiology, Monash University, Melbourne, Victoria, Australia.
Michael FraserOntario Institute for Cancer Research, Toronto, Ontario, Canada.
Richard J RebelloTranslational Oncogenomics Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester Cancer Research Centre, Manchester, UK.
Paul C BoutrosOntario Institute for Cancer Research, Toronto, Ontario, Canada.ORCID http://orcid.org/0000-0003-0553-7520
Declan G MurphySir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Victoria, Australia.ORCID http://orcid.org/0000-0002-7500-5899
Robert G BristowTranslational Oncogenomics Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester Cancer Research Centre, Manchester, UK.ORCID http://orcid.org/0000-0002-8553-9544
Gail P RisbridgerMonash Partners Comprehensive Cancer Consortium and Cancer Program, Biomedicine Discovery Institute, Prostate Cancer Research Group, Department of Anatomy and Developmental Biology and Department of Physiology, Monash University, Melbourne, Victoria, Australia. gail.risbridger@monash.edu.ORCID http://orcid.org/0000-0003-3089-4028
Ontario Institute for Cancer Research · CAUniversity of Manchester · GBDiscovery Institute · USPeter MacCallum Cancer Centre · AUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A key challenge in the management of localized prostate cancer is the identification of men with a high likelihood of progression to an advanced, incurable stage. Patients who harbour germline BRCA2 mutations have worse clinical outcomes than noncarriers when treated with surgery or radiotherapy. Insights from different disciplines have improved our understanding of why patients with BRCA2-mutant tumours have a high likelihood of failing on conventional management after diagnosis. Treatment-naive BRCA2-mutant tumours are defined by aggressive clinical and molecular features early in the disease course, and the genomic landscape of these BRCA2-mutant tumours is characterized by a unique molecular profile and higher genomic instability than noncarrier tumours. Moreover, BRCA2-mutant tumours commonly show the concurrent presence of the intraductal carcinoma of the prostate (IDCP) pathology, a poor prognostic indicator. Subclonal analyses have revealed that IDCP and invasive adenocarcinoma in BRCA2-mutant tumours can arise from the same ancestral clone, implying that a temporal evolutionary trajectory exists. Finally, functional studies have shown that BRCA2-mutant tumours can harbour a subpopulation of cancer cells that can tolerate castration de novo, enabling the tumour to evade androgen deprivation therapy. Importantly, future challenges remain regarding how to best model the biology underpinning this aggressive phenotype and translate these findings to improve clinical outcomes.

Indexed as

MutationBRCA2 ProteinHumansMaleProstatic NeoplasmsBRCA2 ProteinBRCA2 protein, human

Identifiers

PMID30808988
OpenAlexW2915582979

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.