Evidence map›Paper›PMID 35963849›Full record

ArticleCell death discovery2022

Functional antagonism between CagA and DLC1 in gastric cancer.

Isabel Hinsenkamp, Jan P Köhler, Christoph Flächsenhaar, Ivana Hitkova, Sabine Eberhart Meessen, Timo Gaiser, Thomas Wieland, Christel Weiss, Christoph Röcken, Michael Mowat and 8 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2022. 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
0.4field-weighted citation impact, top 37% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Investigation of the Mechanism ofInternational journal of general medicine · 2024
    Article
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 at 5 institutions in 2 countries.

Isabel Hinsenkamp *Department of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Jan P Köhler *Department of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0001-9388-763X
Christoph FlächsenhaarDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Ivana HitkovaDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Sabine Eberhart MeessenDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Timo GaiserInstitute of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Thomas WielandExperimental Pharmacology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0001-8262-8261
Christel WeissDepartment of Medical Statistics and Biomathematics, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0002-8692-5690
Christoph RöckenInstitute of Pathology, Christian Albrechts University Kiel, Kiel, Germany.ORCID http://orcid.org/0000-0002-6989-8002
Michael MowatCancerCare Manitoba Research Institute, Department of Biochemistry & Medical Genetics, University of Manitoba, Winnipeg, MB, Canada.ORCID http://orcid.org/0000-0002-5449-4830
Michael QuanteDepartment of Medicine II, Gastroenterology, Hepatology, Endocrinology, and Infectious Diseases, Faculty of Medicine, University Medical Center Freiburg, Freiburg, Germany.
Karin TaxauerInstitute for Med. Microbiology, Immunology and Hygiene, School of Medicine, Technical University of Munich (TUM), Munich, Germany.
Raquel Mejias-LuqueInstitute for Med. Microbiology, Immunology and Hygiene, School of Medicine, Technical University of Munich (TUM), Munich, Germany.ORCID http://orcid.org/0000-0002-4602-4927
Markus GerhardInstitute for Med. Microbiology, Immunology and Hygiene, School of Medicine, Technical University of Munich (TUM), Munich, Germany.ORCID http://orcid.org/0000-0001-9110-3950
Roger VogelmannDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Nadja Meindl-BeinkerDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Matthias EbertDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Elke BurgermeisterDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. elke.burgermeister@medma.uni-heidelberg.de.ORCID http://orcid.org/0000-0002-4969-5697
Heidelberg University · DETechnical University of Munich · DECancerCare Manitoba · CAChristian-Albrechts-Universität zu Kiel · DEUniversity Medical Center Freiburg · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 410981386Deutsche Forschungsgemeinschaft (German Research Foundation) Bu2285Deutsche Forschungsgemeinschaft (German Research Foundation) GRK2727Deutsche Forschungsgemeinschaft (German Research Foundation) ICONMerck KGaA Merck Heidelberg Innovation Call
6 · The paper itself

Abstract

Helicobacter (H.) pylori-induced gastritis is a risk factor for gastric cancer (GC). Deleted-in-liver-cancer-1 (DLC1/ARHGAP7) inhibits RHOA, a downstream mediator of virulence factor cytotoxin-A (CagA) signalling and driver of consensus-molecular-subtype-2 diffuse GC. DLC1 located to enterochromaffin-like and MIST1+ stem/chief cells in the stomach. DLC1+ cells were reduced in H. pylori gastritis and GC, and in mice infected with H. pylori. DLC1 positivity inversely correlated with tumour progression in patients. GC cells retained an N-terminal truncation variant DLC1v4 in contrast to full-length DLC1v1 in non-neoplastic tissues. H. pylori and CagA downregulated DLC1v1/4 promoter activities. DLC1v1/4 inhibited cell migration and counteracted CagA-driven stress phenotypes enforcing focal adhesion. CagA and DLC1 interacted via their N- and C-terminal domains, proposing that DLC1 protects against H. pylori by neutralising CagA. H. pylori-induced DLC1 loss is an early molecular event, which makes it a potential marker or target for subtype-aware cancer prevention or therapy.

Identifiers

PMID35963849
PMCPMC9376073
OpenAlexW4291202232

What OpenQuestion holds

Textmetadata
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.