Evidence map›Paper›PMID 42680048›Full record

ReviewClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2026

Prevalence and Progression of Subtypes of Gastric Premalignant Lesions: A Systematic Review and Meta-Analysis.

Yendé Grell, Duco T Mülder, Anne I Hahn, Robert J Huang, Margaret J Zhou, Benjamin Blake, Omonefe Omofuma, John D Murphy, Daniela S Gutiérrez-Torres, Ann G Zauber and 8 more

Abstract readReview
In one paragraph

Review in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

18 authors.

Yendé GrellWeill Cornell Medical College of Cornell University, New York, New York.
Duco T MülderDepartment of Public Health, Erasmus Medical Center, Rotterdam, The Netherlands.
Anne I HahnDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
Robert J HuangDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California.
Margaret J ZhouDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California.
Benjamin BlakeWeill Cornell Medical College of Cornell University, New York, New York.
Omonefe OmofumaDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.
John D MurphyDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.
Daniela S Gutiérrez-TorresDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.
Ann G ZauberDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
James F O'MahonyDepartment of Public Health, Erasmus Medical Center, Rotterdam, The Netherlands; School of Economics, University College Dublin, Dublin, Ireland.
M Constanza CamargoDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.
Uri LadabaumDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California.
Jennifer M YehDepartment of Pediatrics, Harvard Medical School, Boston Children's Hospital, Boston, Massachusetts.
Chin HurDivision of General Medicine, Department of Medicine, Columbia University Irving Medical Center, New York, New York; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, New York.
Iris Lansdorp-VogelaarDepartment of Public Health, Erasmus Medical Center, Rotterdam, The Netherlands.
Reinier MeesterDepartment of Public Health, Erasmus Medical Center, Rotterdam, The Netherlands; Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California; Health Economics and Outcomes Research, Freenome Holdings Inc, San Francisco, California.
Monika LaszkowskaGastroenterology, Hepatology, and Nutrition Service, Department of Subspecialty Medicine, Memorial Sloan Kettering Cancer Center, New York, New York. Electronic address: laszkowm@mskcc.org.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Comparative modeling of gastric cancer health drivers and prevention in the US and globallyU01CA265729 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HUR, CHIN, YEH, JENNIFER M. · 2021 to 2025
$4.1M
PRECISE - a PErsonalized Risk Score for gastrIc CancErK08CA252635 · NCI · STANFORD UNIVERSITY · PI HUANG, ROBERT JEFFREY · 2021 to 2025
$941k
A Targeted Approach to the Surveillance of Precursor Lesions for Gastric CancerK08DK125876 · NIDDK · SLOAN-KETTERING INST CAN RESEARCH · PI LASZKOWSKA, MONIKA · 2021 to 2025
$838k
NCI NIH HHS K08 CA252635NCI NIH HHS P30 CA008748NCI NIH HHS U01 CA265729NIDDK NIH HHS K08 DK125876
6 · The paper itself

Abstract

BACKGROUND &

aimsGastric intestinal metaplasia (IM) and dysplasia are precursor lesions for gastric cancer. This systematic review and meta-analysis examined the global prevalence and progression rates of subtypes of these understudied lesions.

methodsWe searched databases for publications reporting prevalence and progression of subtypes of IM and dysplasia among individuals undergoing endoscopy, including incomplete/complete IM, limited (antrum-restricted)/extensive (corpus-involving) IM, and low-grade dysplasia (LGD) and high-grade dysplasia (HGD). Random-effects models were used to estimate pooled prevalence and progression rates to gastric cancer. The I

resultsEighty-three studies were included for prevalence and 23 for progression. The prevalence of complete IM was 11% (95% confidence interval [CI], 8%-15%) and of incomplete IM was 10% (95% CI, 6%-14%), with corresponding progression rates of 1.73 (95% CI, 1.08-2.79) vs 12.15 (95% CI, 5.28-27.94) per 1000 person-years, respectively (P < .01). The prevalence of limited vs extensive IM was 12% (95% CI, 8%-17%) vs 5% (95% CI, 4%-8%), respectively, and the corresponding progression rates were 3.31 (95% CI, 1.18-9.32) vs 4.19 (95% CI, 0.95-18.41) per 1000 person-years (P = .80). The prevalence of LGD was 2% (95% CI, 1%-4%) and of HGD was 0.28% (95% CI, 0.14%-0.55%), with corresponding progression rates of 11.55 (95% CI, 5.93-22.47) vs 344.48 (95% CI, 144.88-819.09; P < .01). Substantial heterogeneity was observed for all estimates.

conclusionsAlthough lesion subtypes with high progression risk like incomplete IM account for a large portion of the total burden of precancerous lesions, subtyping remains underutilized in clinical practice. Although estimates are limited by heterogeneity, differences in progression rates between lesion subtypes support risk stratification of these lesions within management guidelines, particularly complete vs incomplete IM and LGD vs HGD.

Indexed as

DysplasiaGastric CancerIntestinal Metaplasia

Identifiers

PMID42680048
PMCPMC13623031

What OpenQuestion holds

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Registered trials

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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.