Evidence map›Paper›PMID 31804619›Full record

ReviewCellular & molecular immunology2020

Molecular anatomy and pathogenic actions of Helicobacter pylori CagA that underpin gastric carcinogenesis.

Atsushi Takahashi-Kanemitsu, Christopher T Knight, Masanori Hatakeyama

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular & molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 6 pooled it
21.4field-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

179 citing papers in PubMed, 6 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Use of Mendelian Randomization to Unveil Metabolic Markers inJournal of Korean medical science · 2026
    Pooled it
  2. Gastric cancer burden and regional disparities among Helicobacter pylori-positive patients in the Americas: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  10. Microbiology and molecular biology reviews : MMBR · 2026
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  13. [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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119 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

3 authors at 1 institution in 1 country.

Atsushi Takahashi-KanemitsuDepartment of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4156-9522
Christopher T KnightDepartment of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6509-5950
Masanori HatakeyamaDepartment of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. mhata@m.u-tokyo.ac.jp.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic infection with Helicobacter pylori cagA-positive strains is the strongest risk factor for gastric cancer. The cagA gene product, CagA, is delivered into gastric epithelial cells via the bacterial type IV secretion system. Delivered CagA then undergoes tyrosine phosphorylation at the Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs in its C-terminal region and acts as an oncogenic scaffold protein that physically interacts with multiple host signaling proteins in both tyrosine phosphorylation-dependent and -independent manners. Analysis of CagA using in vitro cultured gastric epithelial cells has indicated that the nonphysiological scaffolding actions of CagA cell-autonomously promote the malignant transformation of the cells by endowing the cells with multiple phenotypic cancer hallmarks: sustained proliferation, evasion of growth suppressors, invasiveness, resistance to cell death, and genomic instability. Transgenic expression of CagA in mice leads to in vivo oncogenic action of CagA without any overt inflammation. The in vivo oncogenic activity of CagA is further potentiated in the presence of chronic inflammation. Since Helicobacter pylori infection triggers a proinflammatory response in host cells, a feedforward stimulation loop that augments the oncogenic actions of CagA and inflammation is created in CagA-injected gastric mucosa. Given that Helicobacter pylori is no longer colonized in established gastric cancer lesions, the multistep nature of gastric cancer development should include a "hit-and-run" process of CagA action. Thus, acquisition of genetic and epigenetic alterations that compensate for CagA-directed cancer hallmarks may be required for completion of the "hit-and-run" process of gastric carcinogenesis.

Indexed as

Tumor EscapeAmino Acid MotifsAnimalsAntigens, BacterialBacterial ProteinsHelicobacter InfectionsHelicobacter pyloriHumansNeoplasm InvasivenessStomach NeoplasmsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloricagA/CagAHelicobacter pylori“hit-and-run” carcinogenesisinflammationPAR1SHP2

Identifiers

PMID31804619
PMCPMC6952403
OpenAlexW2992210240

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.