Evidence map›Paper›PMID 16127158›Full record

ArticleThe American journal of pathology2005

The role of antigenic drive and tumor-infiltrating accessory cells in the pathogenesis of helicobacter-induced mucosa-associated lymphoid tissue lymphoma.

Anne Mueller, Jani O'rourke, Pauline Chu, Amanda Chu, Michael F Dixon, Donna M Bouley, Adrian Lee, Stanley Falkow

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

8 authors at 4 institutions in 3 countries.

Anne MuellerDepartment of Microbiology and Immunology, Stanford University Medical School, Stanford, CA 94305, USA. muellera@stanford.edu
Jani O'rourke
Pauline Chu
Amanda Chu
Michael F Dixon
Donna M Bouley
Adrian Lee
Stanley Falkow
Stanford University · USUNSW Sydney · AUStanford Medicine · USUniversity of Leeds · GB

Funding

GENETICS AND CELLULAR BASIS OF H PYLORI PATHOGENESISR01AI038459 · NIAID · STANFORD UNIVERSITY · PI TOMPKINS, LUCY STUART · 1996 to 2010
$4.0M
Helicobacter Host Interactions in Animal ModelsR01CA092229 · NCI · STANFORD UNIVERSITY · PI AMIEVA, MANUEL R · 2001 to 2009
$2.6M
NCI NIH HHS CA92229NCI NIH HHS R01 CA092229NIAID NIH HHS AI38459NIAID NIH HHS R01 AI038459
6 · The paper itself

Abstract

Gastric B-cell lymphoma of mucosa-associated lymphoid tissue type is closely linked to chronic Helicobacter pylori infection. Most clinical and histopathological features of the tumor can be reproduced by prolonged Helicobacter infection of BALB/c mice. In this study, we have addressed the role of antigenic stimulation in the pathogenesis of the lymphoma by experimental infection with Helicobacter felis, followed by antibiotic eradication therapy and subsequent re-infection. Antimicrobial therapy was successful in 75% of mice and led to complete histological but not "molecular" tumor remission. Although lympho-epithelial lesions disappeared and most gastric lymphoid aggregates resolved, transcriptional profiling revealed the long-term mucosal persistence of residual B cells. Experimental re-introduction of Helicobacter led to very rapid recurrence of the lymphomas, which differed from the original lesions by higher proliferative indices and more aggressive behavior. Immunophenotyping of tumor cells revealed massive infiltration of lesions by CD4(+) T cells, which express CD 28, CD 69, and interleukin-4 but not interferon-gamma, suggesting that tumor B-cell proliferation was driven by Th 2-polarized, immunocompetent, and activated T cells. Tumors were also densely colonized by follicular dendritic cells, whose numbers were closely associated with and predictive of treatment outcome.

Indexed as

Helicobacter felisAnimalsAnti-Bacterial AgentsAntigen-Presenting CellsAntigensCD4-Positive T-LymphocytesDendritic CellsDrug Therapy, CombinationFemaleHelicobacter InfectionsLymphoid TissueLymphoma, B-Cell, Marginal ZoneMiceMice, Inbred BALB CMultigene FamilyNeoplasm Recurrence, LocalAnti-Bacterial AgentsAntigens

Identifiers

PMID16127158
PMCPMC1698723
OpenAlexW2021099886

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.