Evidence map›Paper›PMID 40166741›Full record

ArticleArXiv2025

Causes of evolutionary divergence in prostate cancer.

Emre Esentürk, Atef Sahli, Valeriia Haberland, Aleksandra Ziuboniewicz, Christopher Wirth, G Steven Bova, Robert G Bristow, Mark N Brook, Benedikt Brors, Adam Butler and 45 more

Abstract readPreprint
In one paragraph

Article in ArXiv, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

55 authors.

Emre EsentürkNuffield Department of Medicine, University of Oxford, UK.
Atef SahliManchester Cancer Research Centre, The University of Manchester, UK.
Valeriia HaberlandNorwich Medical School, University of East Anglia, UK.
Aleksandra ZiuboniewiczNuffield Department of Surgical Sciences, University of Oxford, UK.
Christopher WirthManchester Cancer Research Centre, The University of Manchester, UK.
G Steven BovaProstate Cancer Research Center, Faculty of Medicine and Health Technology, Tampere University, Finland.
Robert G BristowManchester Cancer Research Centre and Cancer Research UK Manchester Institute, The University of Manchester, UK.
Mark N BrookThe Institute of Cancer Research, UK.
Benedikt BrorsDivision Applied Bioinformatics, German Cancer Research Center (DKFZ), Germany.
Adam ButlerWellcome Sanger Institute, UK.
Géraldine Cancel-TassinCeRePP (Centre de Recherche sur les Pathologies Prostatiques et Urologiques), France.
Kevin Cl ChengComputational Biology Program, Ontario Institute for Cancer Research, Canada.
Colin S CooperNorwich Medical School, University of East Anglia, UK.
Niall M CorcoranDepartment of Urology, Royal Melbourne Hospital, Australia.
Olivier CussenotCeRePP (Centre de Recherche sur les Pathologies Prostatiques et Urologiques), France.
Ros A EelesThe Institute of Cancer Research, UK.
Francesco FaveroBiotech Research & Innovation Centre (BRIC) - University of Copenhagen, Denmark.
Clarissa GerhauserDivision Cancer Epigenomics, German Cancer Research Center (DKFZ), Germany.
Abraham GihawiNorwich Medical School, University of East Anglia, UK.
Etsehiwot G GirmaBiotech Research & Innovation Centre (BRIC) - University of Copenhagen, Denmark.
Vincent J GnanapragasamDepartment of Surgery, Urology, University of Cambridge & Cambridge University Hospitals NHS Trust, Cambridge Urology Translational Research and Clinical Trials (Office), Cambridge Biomedical Campus, Addenbrooke's Hospital Site, S Wards Building, UK.
Andreas J GruberUniversity of Konstanz, Germany.
Anis HamidDepartment of Surgery, The University of Melbourne, Australia.
Vanessa M HayesSchool of Medical Sciences, University of Sydney, Faculty of Medicine & Health, Australia.
Housheng Hansen HePrincess Margaret Cancer Centre, University Health Network; Department of Medical Biophysics, University of Toronto, Canada.
Christopher M HovensDepartment of Surgery, The Collaborative Centre for Genomic Cancer Medicine, The University of Melbourne, Australia.
Eddie Luidy ImadaDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
G Maria JakobsdottirDivision of Cancer Sciences, The University of Manchester, UK.
Chol-Hee JungMelbourne Bioinformatics, The University of Melbourne, Australia.
Francesca KhaniDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
Zsofia Kote-JaraiThe Institute of Cancer Research, UK.
Philippe LamyDepartment of Molecular Medicine, Aarhus University Hospital, Denmark.
Gregory LeemanWellcome Sanger Institute, UK.
Massimo LodaDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
Pavlo LutsikDivision Cancer Epigenomics, German Cancer Research Center (DKFZ), Germany.
Luigi MarchionniDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
Ramyar MolaniaWalter and Eliza Hall Institute of Medical Research, Australia.
Anthony T PapenfussWalter and Eliza Hall Institute of Medical Research, Australia.
Diogo PellegrinaComputational Biology Program, Ontario Institute for Cancer Research, Canada.
Bernard PopeMelbourne Bioinformatics, The University of Melbourne, Australia.
Lucio R QueirozDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
Tobias RauschGenome Biology, European Molecular Biology Laboratory (EMBL), Germany.
Jüri ReimandComputational Biology Program, Ontario Institute for Cancer Research, Canada.
Brian RobinsonDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
Thorsten SchlommDepartment of Urology, Charité - Universitätsmedizin Berlin, Germany.
Karina D SørensenDepartment of Molecular Medicine, Aarhus University Hospital, Denmark.
Sebastian UhrigDivision Applied Bioinformatics, German Cancer Research Center (DKFZ), Germany.
Joachim WeischenfeldtBiotech Research & Innovation Centre (BRIC) - University of Copenhagen, Denmark.
Yaobo XuWellcome Sanger Institute, UK.
Takafumi N YamaguchiJonsson Comprehensive Cancer Center, University of California - Los Angeles, USA.
Claudio ZanettiniDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, USA.
Andy G LynchSchool of Medicine, School of Mathematics & Statistics, University of St Andrews, UK.
David C WedgeManchester Cancer Research Centre, The University of Manchester, UK.
Daniel S BrewerMetabolic Health research centre, Norwich Medical School, University of East Anglia, UK.
Dan J WoodcockNuffield Department of Surgical Sciences, University of Oxford, UK.

Funding

Project 3: Analysis of intrinsic and extrinsic factors that promote prostate neuroendocrine differentiationP01CA265768 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MICHAEL M. SHEN · 2022 to 2026
$13.4M
Weill Cornell Medicine (WCM) SPORE in Prostate CancerP50CA211024 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI RICKMAN, DAVID S. · 2017 to 2021
$10.9M
Genomic Diversity of Prostate Cancer Across the African DiasporaR01CA259200 · NCI · DANA-FARBER CANCER INST · PI TIMOTHY RICHARD REBBECK · 2022 to 2026
$6.4M
Genomic bases for African geo-ethnic prostate cancer health disparityR01CA285772 · NCI · UNIVERSITY OF SYDNEY · PI Vanessa Marie Hayes · 2024 to 2026
$1.5M
NCI NIH HHS P01 CA265768NCI NIH HHS P50 CA211024NCI NIH HHS R01 CA259200NCI NIH HHS R01 CA285772
6 · The paper itself

Abstract

Cancer progression involves the sequential accumulation of genetic alterations that cumulatively shape the tumour phenotype. In prostate cancer, tumours can follow divergent evolutionary trajectories that lead to distinct subtypes, but the causes of this divergence remain unclear. While causal inference could elucidate the factors involved, conventional methods are unsuitable due to the possibility of unobserved confounders and ambiguity in the direction of causality. Here, we propose a method that circumvents these issues and apply it to genomic data from 829 prostate cancer patients. We identify several genetic alterations that drive divergence as well as others that prevent this transition, locking tumours into one trajectory. Further analysis reveals that these genetic alterations may cause each other, implying a positive-feedback loop that accelerates divergence. Our findings provide insights into how cancer subtypes emerge and offer a foundation for genomic surveillance strategies aimed at monitoring the progression of prostate cancer.

Indexed as

cancer evolutioncausal inferencecausalityevolutionary divergenceprostate cancer

Identifiers

PMID40166741
PMCPMC11957227

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.