Evidence map›Paper›PMID 36131292›Full record

ArticleMolecular cancer2022

The architecture of clonal expansions in morphologically normal tissue from cancerous and non-cancerous prostates.

Claudia Buhigas, Anne Y Warren, Wing-Kit Leung, Hayley C Whitaker, Hayley J Luxton, Steve Hawkins, Jonathan Kay, Adam Butler, Yaobo Xu, Dan J Woodcock and 17 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

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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

27 authors at 15 institutions in 4 countries.

Claudia BuhigasNorwich Medical School, University of East Anglia, Norwich, Norfolk, NR4 7TJ, UK.
Anne Y WarrenDepartment of Histopathology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, CB2 0QQ, UK.
Wing-Kit LeungCancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Hayley C WhitakerCancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Hayley J LuxtonCancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Steve HawkinsCancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Jonathan KayCancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Adam ButlerCancer, Ageing and Somatic Mutation, Wellcome Trust Sanger Institute, Hinxton, CB10 1RQ, UK.
Yaobo XuCancer, Ageing and Somatic Mutation, Wellcome Trust Sanger Institute, Hinxton, CB10 1RQ, UK.
Dan J WoodcockOxford Big Data Institute, University of Oxford, Old Road Campus, Oxford, OX3 7LF, UK.
Sue MersonThe Institute of Cancer Research, London, SW7 3RP, UK.
Fiona M FrameCancer Research Unit, Department of Biology, University of York, Heslington, YO10 5DD, North Yorkshire, UK.
Atef SahliOxford Big Data Institute, University of Oxford, Old Road Campus, Oxford, OX3 7LF, UK.
Federico AbascalCancer, Ageing and Somatic Mutation, Wellcome Trust Sanger Institute, Hinxton, CB10 1RQ, UK.
CRUK-ICGC Prostate Cancer Group
Iñigo MartincorenaCancer, Ageing and Somatic Mutation, Wellcome Trust Sanger Institute, Hinxton, CB10 1RQ, UK.
G Steven BovaFaculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, 33014, Tampere, FI, Finland.
Christopher S FosterHCA Laboratories, London, WC1E 6JA, UK.
Peter CampbellCancer, Ageing and Somatic Mutation, Wellcome Trust Sanger Institute, Hinxton, CB10 1RQ, UK.
Norman J MaitlandCancer Research Unit, Department of Biology, University of York, Heslington, YO10 5DD, North Yorkshire, UK.
David E NealCancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Charlie E Massie *Cancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Andy G Lynch *Cancer Research UK Cambridge Institute, Cambridge, CB2 0RE, UK.
Rosalind A Eeles *The Institute of Cancer Research, London, SW7 3RP, UK.
Colin S Cooper *Norwich Medical School, University of East Anglia, Norwich, Norfolk, NR4 7TJ, UK.
David C Wedge *Oxford Big Data Institute, University of Oxford, Old Road Campus, Oxford, OX3 7LF, UK.
Daniel S Brewer *Norwich Medical School, University of East Anglia, Norwich, Norfolk, NR4 7TJ, UK. d.brewer@uea.ac.uk.
University of East Anglia · GBRoyal Marsden NHS Foundation Trust · GBWellcome Sanger Institute · GBCancer Research UK Cambridge Center · GBInstitute of Cancer Research · GBCambridge University Hospitals NHS Foundation Trust · GBTampere University · FIUniversity of Manchester · GBUniversity of Oxford · GBEarlham Institute · GBHutchison/MRC Research Centre · GBUniversity of Cambridge · GBYorkshire Cancer Research · GBUniversity College London · GBUniversity of St Andrews · GB

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Cancer Research UK 21777Cancer Research UK C5047/A29626/A22530/A17528EPA EP-C-15-003Medical Research Council G0500966NCI NIH HHS P30 CA047904Wellcome Trust
6 · The paper itself

Abstract

backgroundUp to 80% of cases of prostate cancer present with multifocal independent tumour lesions leading to the concept of a field effect present in the normal prostate predisposing to cancer development. In the present study we applied Whole Genome DNA Sequencing (WGS) to a group of morphologically normal tissue (n = 51), including benign prostatic hyperplasia (BPH) and non-BPH samples, from men with and men without prostate cancer. We assess whether the observed genetic changes in morphologically normal tissue are linked to the development of cancer in the prostate.

resultsSingle nucleotide variants (P = 7.0 × 10

conclusionsCells within regions of morphologically normal tissue (both BPH and non-BPH) can expand under selective pressure by mechanisms that are distinct from those occurring in adjacent cancer, but that are allied to the presence of cancer. Expansions, which are probably stromal in origin, are characterised by lack of recurrent driver mutations, by almost complete absence of structural variants/copy number alterations, and mutational processes similar to malignant tissue. Our findings have implications for treatment (focal therapy) and early detection approaches.

Indexed as

Prostatic HyperplasiaProstatic NeoplasmsClone CellsHumansMaleNucleotidesProstateNucleotidesBenign prostatic hyperplasiaClonal expansionsField effectGenomicsMutational signaturesNormal tissueProstate cancer

Identifiers

PMID36131292
PMCPMC9494848
OpenAlexW4296793877

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.