Evidence map›Paper›PMID 21611816›Full record

ReviewLangenbeck's archives of surgery2011

Gastric carcinogenesis.

Jan Bornschein, Peter Malfertheiner

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Langenbeck's archives of surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
7.7field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. ANKRD1 expression and functional mechanism in stomach adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. Article
  4. Review
  5. Role of microRNA-494 in tumor progression.American journal of translational research · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Toll-like receptor 2 and 4 polymorphisms associated with Helicobacter pylori susceptibility and gastric cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Helicobacter pylori in gastric carcinogenesis.World journal of gastrointestinal oncology · 2015
    Review
  16. IsBariatric surgical practice and patient care · 2015
    Article
  17. Correlation analysis of riboflavin, RFT2 and Helicobater pylori in gastric carcinoma.International journal of clinical and experimental pathology · 2015
    Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Jan BornscheinDepartment of Gastroenterology, Hepatology & Infectious Diseases, Otto-von-Guericke University of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany.
Peter Malfertheiner
Otto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIn most patients, gastric cancer is diagnosed in advanced stage. Curative treatment options are limited and the mortality is high. The process of gastric carcinogenesis is triggered by Helicobacter pylori-driven gastritis and is further characterized by its complexity of interaction with other risk factors. Health care systems are challenged for the improvement of prevention, early diagnosis, and effective treatments.

methodsAn extensive literature research has been performed to elucidate the interplay between etiological factors involved in gastric carcinogenesis.

resultsH. pylori is the most important carcinogen for gastric adenocarcinoma. Evidence is provided by experiments including animal studies as well as clinical observational and interventional studies in humans. Eradication has the potential to prevent gastric cancer and offers the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of the carcinogenesis in the stomach. Host genetic factors contribute to the regulation of the inflammatory response and in the aggravation of mucosal damage. The harmful role of environmental factors is restricted to salt intake and smoking of tobacco. The ingestion of fruit and vegetables has some protective effect.

conclusionInfection with H. pylori is the major risk factor for gastric cancer development, and thus, eradication of the Helicobacter offers a promising best option for prevention of the disease. Bacterial virulence, host genetic factors, and environmental influences are interacting in the multifactorial process of gastric carcinogenesis.

Indexed as

AnimalsAnti-Bacterial AgentsCyclooxygenase 2 InhibitorsEarly DiagnosisHelicobacter InfectionsHelicobacter pyloriHumansPrecancerous ConditionsStomach NeoplasmsAnti-Bacterial AgentsCyclooxygenase 2 Inhibitors

Identifiers

PMID21611816
OpenAlexW3190119538

What OpenQuestion holds

Textmetadata
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.