Evidence map›Paper›PMID 39880602›Full record

ArticleGut2025

Low-coverage whole genome sequencing of low-grade dysplasia strongly predicts advanced neoplasia risk in ulcerative colitis.

Ibrahim Al Bakir, Kit Curtius, George D Cresswell, Heather E Grant, Nadia Nasreddin, Kane Smith, Salpie Nowinski, Qingli Guo, Hayley L Belnoue-Davis, Jennifer Fisher and 15 more

Abstract readMulticenter Study
In one paragraph

Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Pathophysiology of colitis-associated colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors.

Ibrahim Al BakirBarts Cancer Institute, Queen Mary University of London, London, UK.
Kit CurtiusBarts Cancer Institute, Queen Mary University of London, London, UK kcurtius@health.ucsd.edu simon.leedham@well.ox.ac.uk ailsa.hart@nhs.net trevor.graham@icr.ac.uk.
George D CresswellCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0003-3303-068X
Heather E GrantCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
Nadia NasreddinWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Kane SmithBarts Cancer Institute, Queen Mary University of London, London, UK.
Salpie NowinskiBarts Cancer Institute, Queen Mary University of London, London, UK.
Qingli GuoBarts Cancer Institute, Queen Mary University of London, London, UK.
Hayley L Belnoue-DavisWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Jennifer FisherInflammatory Bowel Disease Unit, St Mark's Hospital, Harrow, UK.
Theo ClarkeBarts Cancer Institute, Queen Mary University of London, London, UK.
Christopher KimberleyBarts Cancer Institute, Queen Mary University of London, London, UK.
Maximilian MossnerBarts Cancer Institute, Queen Mary University of London, London, UK.
Philip D DunneCentre for Cancer Research and Cell Biology, Queens University Belfast, Belfast, UK.ORCID 0000-0001-9160-283X
Maurice B LoughreyCellular Pathology, Belfast Health and Social Care Trust, Belfast, UK.ORCID 0000-0001-8424-1765
Ally SpeightDepartment of Gastroenterology, Newcastle upon Tyne Hospitals NHS Trust, Newcastle upon Tyne, UK.
James E EastTranslational Gastroenterology Unit, Nuffield Department of Medicine, John Radcliffe Hospital, Univerity of Oxford, Oxford, UK.ORCID 0000-0001-8035-3700
Nicholas A WrightBarts Cancer Institute, Queen Mary University of London, London, UK.
Manuel Rodriguez-JustoDepartment of Pathology, University College London Hospital, London, UK.
Marnix JansenDepartment of Pathology, University College London Hospital, London, UK.
Morgan MoorghenDepartment of Histopathology, St Mark's Hospital, Harrow, UK.
Ann-Marie BakerBarts Cancer Institute, Queen Mary University of London, London, UK.
Simon J LeedhamWellcome Centre for Human Genetics, University of Oxford, Oxford, UK kcurtius@health.ucsd.edu simon.leedham@well.ox.ac.uk ailsa.hart@nhs.net trevor.graham@icr.ac.uk.
Ailsa L HartInflammatory Bowel Disease Unit, St Mark's Hospital, Harrow, UK kcurtius@health.ucsd.edu simon.leedham@well.ox.ac.uk ailsa.hart@nhs.net trevor.graham@icr.ac.uk.
Trevor A GrahamBarts Cancer Institute, Queen Mary University of London, London, UK kcurtius@health.ucsd.edu simon.leedham@well.ox.ac.uk ailsa.hart@nhs.net trevor.graham@icr.ac.uk.ORCID 0000-0001-9582-1597

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
San Diego Digestive Diseases Research CenterP30DK120515 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bernd G. Schnabl · 2019 to 2026
$10.8M
Multiscale modeling of spatiotemporal evolution in Barrett's esophagusR01CA270235 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Kathleen M. Curtius · 2023 to 2026
$2.3M
BLRD VA I01 BX005958NCI NIH HHS P30 CA023100NCI NIH HHS R01 CA270235NIDDK NIH HHS P30 DK120515
6 · The paper itself

Abstract

backgroundThe risk of developing advanced neoplasia (AN; colorectal cancer and/or high-grade dysplasia) in ulcerative colitis (UC) patients with a low-grade dysplasia (LGD) lesion is variable and difficult to predict. This is a major challenge for effective clinical management.

objectiveWe aimed to provide accurate AN risk stratification in UC patients with LGD. We hypothesised that the pattern and burden of somatic genomic copy number alterations (CNAs) in LGD lesions could predict future AN risk.

designWe performed a retrospective multicentre validated case-control study using n=270 LGD samples from n=122 patients with UC. Patients were designated progressors (n=40) if they had a diagnosis of AN in the ~5 years following LGD diagnosis or non-progressors (n=82) if they remained AN-free during follow-up. DNA was extracted from the baseline LGD lesion, low-coverage whole genome sequencing performed and data processed to detect CNAs. Survival analysis was used to evaluate CNAs as predictors of future AN risk.

resultsCNA burden was significantly higher in progressors than non-progressors (p=2×10

conclusionMeasurement of CNAs in LGD is an accurate predictor of AN risk in inflammatory bowel disease and is likely to support clinical management.

Indexed as

Colitis, UlcerativeColorectal NeoplasmsWhole Genome SequencingAdultAgedCase-Control StudiesDisease ProgressionDNA Copy Number VariationsFemaleHumansMaleMiddle AgedRetrospective StudiesRisk AssessmentRisk FactorsCANCER PREVENTIONCOLORECTAL CANCERGENETIC INSTABILITYINFLAMMATORY BOWEL DISEASEULCERATIVE COLITIS

Identifiers

PMID39880602
PMCPMC12013573

What OpenQuestion holds

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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.