Evidence map›Paper›PMID 31332522›Full record

ArticleVirchows Archiv : an international journal of pathology2019

Expression of the potential therapeutic target claudin-18.2 is frequently decreased in gastric cancer: results from a large Caucasian cohort study.

Matthias Dottermusch, Sandra Krüger, Hans-Michael Behrens, Christine Halske, Christoph Röcken

Open access · hybridAbstract read
In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 6% 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

89 citing papers in PubMed, 3 syntheses or guidelines pooled it, 125 citations in OpenAlex.

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29 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

5 authors at 1 institution in 1 country.

Matthias DottermuschDepartment of Pathology, Christian-Albrechts-University, Arnold-Heller-Str. 3, Haus 14, 24105, Kiel, Germany.
Sandra KrügerDepartment of Pathology, Christian-Albrechts-University, Arnold-Heller-Str. 3, Haus 14, 24105, Kiel, Germany.
Hans-Michael BehrensDepartment of Pathology, Christian-Albrechts-University, Arnold-Heller-Str. 3, Haus 14, 24105, Kiel, Germany.
Christine HalskeDepartment of Pathology, Christian-Albrechts-University, Arnold-Heller-Str. 3, Haus 14, 24105, Kiel, Germany.
Christoph RöckenDepartment of Pathology, Christian-Albrechts-University, Arnold-Heller-Str. 3, Haus 14, 24105, Kiel, Germany. christoph.roecken@uksh.de.ORCID http://orcid.org/0000-0002-6989-8002
Christian-Albrechts-Universität zu Kiel · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is frequently diagnosed and treated in advanced tumour stages with poor prognosis. Recent studies have identified isoform 2 of the tight junction protein claudin-18 (CLDN18.2) as a promising target in GC therapy. In this study, we aimed to outline the expression of CLDN18.2 and its correlation with clinico-pathological patient characteristics in a large and well-characterized cohort of GC patients. The expression of CLDN18.2 was studied in 481 GCs by immunohistochemistry on whole tissue sections. Immunostained GCs were evaluated using the histoscore (H-score) and subsequently divided into two groups: tumours showing any or no expression. CLDN18.2 expression was investigated for correlation with various clinico-pathological patient characteristics, including survival. CLDN18.2 expression was found in 203 GCs (42.2%). Of these tumours, 71 (14.8%) showed solely weak immunostaining. CLDN18.2 expression correlated with mucin phenotype, EBV status, the integrin αvβ5, the EpCAM extracellular domain EpEX, and lysozyme. We found no correlation with survival, Laurén phenotype, or any other clinico-pathological patient characteristic. In conclusion, we demonstrate frequently decreased expression of CLDN18.2 in a GC cohort of appropriate size. Correlating CLDN18.2 expression with clinico-pathological patient characteristics reveals new linkages to αvβ5, EpEX, and lysozyme, which may pave the way for further investigations regarding the role of tight junction proteins in GC progression. Though CLDN18.2 continues to pose an attractive target candidate, we conclude that a rather low overall expression rate challenges its significance in advanced GC therapy and indicates the need for further investigations across different populations.

Indexed as

AgedClaudinsCohort StudiesEpithelial Cell Adhesion MoleculeFemaleHumansImmunohistochemistryMaleMucinsMuramidaseNeoplasm StagingPhenotypePrognosisStomach NeoplasmsTight JunctionsWhite PeopleClaudinsCLDN18 protein, humanEPCAM protein, humanEpithelial Cell Adhesion MoleculeMucinsMuramidaseClaudin-18.2EBVGastric cancerPrognosisStomach neoplasmsTight junctions

Identifiers

PMID31332522
PMCPMC6861347
OpenAlexW2963441600

What OpenQuestion holds

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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.