Evidence map›Paper›PMID 18321303›Full record

ArticleHelicobacter2008

Helicobacter pylori genotyping and sequencing using paraffin-embedded biopsies from residents of colombian areas with contrasting gastric cancer risks.

Liviu A Sicinschi, Pelayo Correa, Richard M Peek, M Constanza Camargo, Alberto Delgado, M Blanca Piazuelo, Judith Romero-Gallo, Luis E Bravo, Barbara G Schneider

Abstract read
In one paragraph

Article in Helicobacter, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Effect of treatment failure on the CagA EPIYA motif inWorld journal of gastroenterology · 2017
    Trial
  2. DNA Methylation Predicts Progression of Human Gastric Lesions.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2015
    Trial
  3. Trial
  4. Virulence Genes ofCanadian journal of gastroenterology & hepatology · 2022
    Article
  5. Article
  6. Article
  7. Saudi journal of biological sciences · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Gastric cancer: an infectious disease.Infectious disease clinics of North America · 2010
    Review
  16. CagA C-terminal variations in Helicobacter pylori strains from Colombian patients with gastric precancerous lesions.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2010
    Article
  17. Article
  18. Article
  19. Natural history of Helicobacter pylori infection.Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2008
    Article
  20. Detection and Genotyping ofPakistan journal of medical sciences
    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

9 authors at 2 institutions in 2 countries.

Liviu A SicinschiDivision of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA. liviu.sicinschi@Vanderbilt.edu
Pelayo Correa
Richard M Peek
M Constanza Camargo
Alberto Delgado
M Blanca Piazuelo
Judith Romero-Gallo
Luis E Bravo
Barbara G Schneider
Vanderbilt University · USUniversidad del Valle · CO

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Role of Iron and B-Catenin Activation in Gastric CarcinogenesisP01CA116087 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2009 to 2026
$27.5M
Project 3 - Molecular Signatures of Gastric Carcinogenesis in the Host Response to H. pyloriP01CA028842 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, KEITH T. · 1985 to 2019
$15.8M
H.Pylori Relationship to Digestive Diseases and CancerR01CA077955 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2003 to 2026
$9.7M
Helicobacter Pylori and Gastrointestinal BiologyR01DK058587 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEK, RICHARD M. · 2001 to 2024
$7.8M
Mechanism that regulate Helicobacter pylori-induced beta-caterin activationR01DK073902 · NIDDK · VANDERBILT UNIVERSITY · PI PEEK, RICHARD M. · 2006 to 2009
$1.2M
NCI NIH HHS P01 CA028842NCI NIH HHS P01 CA116087NCI NIH HHS P01 CA 28842NCI NIH HHS R01 CA077955NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK058587NIDDK NIH HHS R01 DK073902NIDDK NIH HHS R01 DK58587NIDDK NIH HHS R01 DK 73902PHS HHS R01 A77955
6 · The paper itself

Abstract

backgroundcagA-positive and vacA s1 and m1 genotypes of Helicobacter pylori are associated with an elevated risk of gastric cancer (GC). We determined these genotypes using paraffin-embedded gastric biopsy specimens harvested from infected individuals and compared genotype distributions in two Colombian populations residing in geographic regions with a high and low incidence of GC.

methodsDNA from paraffin-embedded gastric biopsies from 107 adults was amplified using primers specific for cagA, for the cag'empty site', for the s and m alleles of vacA, and for H. pylori 16S rRNA.

resultsH. pylori infection was detected by molecular assays in 97 (90.7%) biopsies. Complete genotyping of cagA and vacA was achieved in 94 (96.9%) cases. The presence of cagA was detected in 78 of 97 cases (80.4%); when considered separately, cagA and vacA s regions were not significantly associated with a particular geographic area. The vacA m1 allele and s1m1 genotypes were more common in the area of high risk for GC (p = .037 and p = .044, respectively), while the vacA m2 allele and s2m2 genotypes were more prevalent in the low-risk area. The prevalence of the combination of cagA-positive, vacA s1m1 genotypes was 84.3% and 60.5% for high and low risk areas, respectively (p = .011).

conclusionsH. pylori cagA and vacA genotyping from paraffin-embedded gastric biopsies permitted reliable typability and discrimination. The more virulent cagA-positive s1m1 strains, as well as vacA m1 genotype, were more prevalent in high risk than in low risk areas, which may contribute to the difference in GC risk between those two regions.

Indexed as

Bacterial Typing TechniquesAdultAntigens, BacterialBacterial ProteinsBiopsyDNA, BacterialGastritisGenotypeHelicobacter InfectionsHelicobacter pyloriHumansParaffin EmbeddingStomach NeoplasmsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriDNA, BacterialVacA protein, Helicobacter pylori

Identifiers

PMID18321303
PMCPMC2977907
OpenAlexW1998948527

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.