Evidence map›Paper›PMID 34797436›Full record

SynthesisCancer causes & control : CCC2022

The risk of diffuse-type gastric cancer following diagnosis with gastric precancerous lesions: a systematic review and meta-analysis.

John E Wang, Sung Eun Kim, Bong Eun Lee, Sungho Park, Joo Ha Hwang, Robert J Huang

Open access · greenAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Cancer causes & control : CCC, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 2 institutions in 1 country.

John E WangDepartment of Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Sung Eun KimDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, 300 Pasteur Drive, Alway Building, M211, Stanford, CA, 94305, USA.
Bong Eun LeeDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, 300 Pasteur Drive, Alway Building, M211, Stanford, CA, 94305, USA.
Sungho ParkDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, 300 Pasteur Drive, Alway Building, M211, Stanford, CA, 94305, USA.
Joo Ha HwangDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, 300 Pasteur Drive, Alway Building, M211, Stanford, CA, 94305, USA.
Robert J HuangDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, 300 Pasteur Drive, Alway Building, M211, Stanford, CA, 94305, USA. rjhuang@stanford.edu.ORCID http://orcid.org/0000-0002-0891-7409
Stanford University · USStanford Medicine · US

Funding

PRECISE - a PErsonalized Risk Score for gastrIc CancErK08CA252635 · NCI · STANFORD UNIVERSITY · PI HUANG, ROBERT JEFFREY · 2021 to 2025
$941k
NCI NIH HHS K08 CA252635NCI NIH HHS K08CA252635
6 · The paper itself

Abstract

purposeGastric cancers are classified as diffuse-type (DTGC) or intestinal-type (ITGC). DTGCs have distinct clinical and histopathologic features, and carry a worse overall prognosis compared to ITGCs. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known precursors to ITGC. It is unknown if AG and IM increase risk for DTGC.

methodsWe performed a systematic review to identify studies reporting on the association of AG/IM and DTGC. We extracted the odds ratio (OR) of the association from studies, and performed pool analysis. Subgroup analysis was performed on studies reporting histologic severity (using operative link systems) to assess if histologic severity of AG/IM was associated with higher risk.

resultsWe identified six case-control and eight cohort studies for inclusion. Both AG (pooled OR = 1.9, 95% CI 1.5 to 2.4, p < 0.001) and IM (pooled OR = 2.3, 95% CI 1.9 to 2.9, p < 0.001) demonstrated an association with DTGC. High AG severity was associated with increased risk for DTGC compared to low AG severity (OR = 1.7, 95% CI 1.2 to 2.3, p = 0.002). Similarly, high IM severity was associated with increased risk compared to low IM severity (OR = 1.9, 95% CI 1.3 to 2.7, p = 0.001).

conclusionBoth AG and IM are associated with DTGC. Increasing histologic severity of both AG and IM increases risk for DTGC. There may exist a common pathway between ITGC and some DTGCs mediated through mucosal precursor lesions. These data may inform future strategies of cancer risk attenuation and control.

Indexed as

Gastritis, AtrophicHelicobacter InfectionsHelicobacter pyloriPrecancerous ConditionsStomach NeoplasmsGastric MucosaHumansMetaplasiaRisk FactorsAtrophic gastritisHelicobacter pyloriIntestinal metaplasiaPrevention

Identifiers

PMID34797436
PMCPMC8776597
OpenAlexW3211713592

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.