Evidence map›Paper›PMID 35288702›Full record

ReviewNature reviews. Gastroenterology & hepatology2022

The immune microenvironment in gastric adenocarcinoma.

Yana Zavros, Juanita L Merchant

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 2 pooled it
30.7field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 2 syntheses or guidelines pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Frontiers in medicine · 2024
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57 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Yana ZavrosDepartment of Cellular and Molecular Medicine and Department of Medicine, Division of Gastroenterology and Hepatology, University of Arizona, Tucson, AZ, USA.
Juanita L MerchantDepartment of Cellular and Molecular Medicine and Department of Medicine, Division of Gastroenterology and Hepatology, University of Arizona, Tucson, AZ, USA. jmerchant@arizona.edu.
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
Uranium as an Environmental Risk Factor for Cancer Among the NavajoU54CA143924 · NCI · UNIVERSITY OF ARIZONA · PI Melissa Marie Herbst-Kralovetz, JUANITA L. MERCHANT · 2009 to 2026
$26.7M
The role of Hedgehog Signaling in gastric tissue repair and regenerationR01DK083402 · NIDDK · UNIVERSITY OF CINCINNATI · PI ZAVROS, YANA · 2011 to 2019
$3.7M
MDSC Polarization and Helicobacter-Induced Gastric MetaplasiaR01DK118563 · NIDDK · UNIVERSITY OF ARIZONA · PI MERCHANT, JUANITA L. · 2018 to 2021
$1.4M
NCI NIH HHS P30 CA023074NCI NIH HHS U54 CA143924NIDDK NIH HHS R01 DK083402NIDDK NIH HHS R01 DK118563
6 · The paper itself

Abstract

Like most solid tumours, the microenvironment of epithelial-derived gastric adenocarcinoma (GAC) consists of a variety of stromal cell types, including fibroblasts, and neuronal, endothelial and immune cells. In this article, we review the role of the immune microenvironment in the progression of chronic inflammation to GAC, primarily the immune microenvironment driven by the gram-negative bacterial species Helicobacter pylori. The infection-driven nature of most GACs has renewed awareness of the immune microenvironment and its effect on tumour development and progression. About 75-90% of GACs are associated with prior H. pylori infection and 5-10% with Epstein-Barr virus infection. Although 50% of the world's population is infected with H. pylori, only 1-3% will progress to GAC, with progression the result of a combination of the H. pylori strain, host susceptibility and composition of the chronic inflammatory response. Other environmental risk factors include exposure to a high-salt diet and nitrates. Genetically, chromosome instability occurs in ~50% of GACs and 21% of GACs are microsatellite instability-high tumours. Here, we review the timeline and pathogenesis of the events triggered by H. pylori that can create an immunosuppressive microenvironment by modulating the host's innate and adaptive immune responses, and subsequently favour GAC development.

Indexed as

AdenocarcinomaEpstein-Barr Virus InfectionsHelicobacter InfectionsHelicobacter pyloriStomach NeoplasmsGastric MucosaHerpesvirus 4, HumanHumansInflammationTumor Microenvironment

Identifiers

PMID35288702
PMCPMC9809534
OpenAlexW4220661700

What OpenQuestion 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 OpenQuestion graph.