Evidence map›Paper›PMID 28322182›Full record

ReviewExpert reviews in molecular medicine2017

Helicobacter pylori as an oncogenic pathogen, revisited.

Muhammad Miftahussurur, Yoshio Yamaoka, David Y Graham

Open access · greenAbstract readReview
In one paragraph

Review in Expert reviews in molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 83 citations in OpenAlex.

  1. Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026
    Review
  2. Allelic Variation ofMicroorganisms · 2025
    Article
  3. Helicobacter pylori Infection in Colombia: Phylogeny, Resistome, and Virulome.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Microorganisms · 2024
    Review
  8. Helicobacter pylori.Current topics in microbiology and immunology · 2024
    Review
  9. Pivotal role ofFrontiers in medicine · 2024
    Review
  10. Influence ofWorld journal of clinical oncology · 2022
    Review
  11. Characterization and Genomic Analysis of a New Phage InfectingInternational journal of molecular sciences · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Observational
  16. International journal of molecular sciences · 2021
    Review
  17. Review
  18. Hippo-YAP signaling in digestive system tumors.American journal of cancer research · 2021
    Review
  19. Article
  20. The Journal of biological chemistry · 2020
    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

3 authors at 1 institution in 1 country.

Muhammad MiftahussururDepartment of Medicine,Gastroenterology and Hepatology Section,Baylor College of Medicine,Houston,Texas 77030,USA.
Yoshio YamaokaDepartment of Medicine,Gastroenterology and Hepatology Section,Baylor College of Medicine,Houston,Texas 77030,USA.
David Y GrahamDepartment of Medicine,Gastroenterology and Hepatology Section,Baylor College of Medicine,Houston,Texas 77030,USA.
Baylor College of Medicine · US

Funding

Tissue Analysis & Molecular Imaging CoreP30DK056338 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI James Versalovic · 2001 to 2026
$28.3M
REGULATION OF CXC CHEMOKINE EXPRESSION BY H. PYLORIR01DK062813 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI YAMAOKA, YOSHIO · 2004 to 2013
$3.0M
NIDDK NIH HHS P30 DK056338NIDDK NIH HHS R01 DK062813
6 · The paper itself

Abstract

Gastric cancer is an inflammation-associated malignancy aetiologically related to infection with the bacterium, Helicobacter pylori, which is considered a necessary but insufficient cause. Unless treated, H. pylori causes life-long acute and chronic gastric inflammation resulting in progressive gastric mucosal damage that may result in gastric cancer. The rate of progression from superficial gastritis, to an atrophic metaplastic mucosa, and ultimately to cancer relates to the virulence of the infecting H. pylori as well as host and environmental factors. H. pylori virulence is a reflection of its propensity to cause severe gastric inflammation. Both mucosal inflammation and H. pylori can cause host genomic instability, including dysregulation of DNA mismatch repair, stimulation of expression of activation-induced cytidine deaminase, abnormal DNA methylation and dysregulation of  micro RNAs, which may result in an accumulation of mutations and loss of normal regulation of cell growth. The difference in cancer risk between the most and least virulent H. pylori strain is only approximately 2-fold. Overall, none of the putative virulence factors identified to date have proved to be disease-specific. The presence, severity, extent and duration of inflammation appear to be the most important factors and current evidence suggests that any host, environmental or bacterial factor that reliably enhances the inflammatory response to the H. pylori infection increases the risk of gastric cancer.

Indexed as

Cell Transformation, NeoplasticHost-Pathogen InteractionsAnimalsAntigens, BacterialBacterial ProteinsDisease SusceptibilityGenomic InstabilityHelicobacter InfectionsHelicobacter pyloriHumansMicrobiotaNeoplasmsOncogene ProteinsResearchVirulence FactorsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriOncogene ProteinsVirulence Factors

Identifiers

PMID28322182
PMCPMC6905048
OpenAlexW2603672279

What OpenQuestion holds

Textmetadata
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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.