Evidence map›Paper›PMID 10948161›Full record

ArticleInfection and immunity2000

Chronic Helicobacter pylori infection induces an apoptosis-resistant phenotype associated with decreased expression of p27(kip1).

H Shirin, E M Sordillo, T K Kolevska, H Hibshoosh, Y Kawabata, S H Oh, J F Kuebler, T Delohery, C M Weghorst, I B Weinstein and 1 more

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.8field-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

25 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Interface-Based Structural Prediction of Novel Host-Pathogen Interactions.Methods in molecular biology (Clifton, N.J.) · 2019
    Article
  4. Structural host-microbiota interaction networks.PLoS computational biology · 2017
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Rodent models of Helicobacter infection, inflammation, and disease.Methods in molecular biology (Clifton, N.J.) · 2012
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. p27kip1 expression is inversely related to the grade of gastric MALT lymphoma.International journal of gastrointestinal cancer · 2005
    Article
  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

11 authors at 5 institutions in 2 countries.

H ShirinDepartment of Medicine, St. Luke's-Roosevelt Hospital Center, College of Physicians and Surgeons, Columbia University, New York, New York 10025, USA.
E M Sordillo
T K Kolevska
H Hibshoosh
Y Kawabata
S H Oh
J F Kuebler
T Delohery
C M Weghorst
I B Weinstein
S F Moss
Herbert Irving Comprehensive Cancer CenterColumbia University · USMemorial Sloan Kettering Cancer Center · USSt. Luke's-Roosevelt Hospital Center · USThe Ohio State University · US

Funding

CYCLIN GENES AND MULTISTAGE CARCINOGENESISR01CA063467 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI WEINSTEIN, I. BERNARD · 1995 to 1999
–
NCI NIH HHS R01CA63467
6 · The paper itself

Abstract

Helicobacter pylori infection is associated with the development of gastric cancer. In short-term coculture with AGS gastric cells, H. pylori inhibits cell cycle progression and induces dose-dependent apoptosis. Based on the concept that an imbalance between proliferation and apoptosis may contribute to the emergence of gastric cancer, we chronically exposed AGS cells to H. pylori as a model of chronic exposure in humans. The AGS derivatives selected by this process were stably resistant not only to H. pylori-induced apoptosis but also to apoptosis induced by other enteric bacteria and by several toxic agents including radiation and cancer chemotherapy. Like the parental AGS cells, the derivatives underwent G(1)/S-phase cell cycle inhibition in response to H. pylori. The AGS derivatives displayed a marked decrease in cellular levels of the cell cycle control protein p27(kip1). We found a similar decrease in epithelial cell p27(kip1) expression in gastric biopsy specimens from H. pylori-infected patients. These findings are consistent with observations that link decreases in the p27(kip1) level to increased susceptibility to cancer in mice with p27(kip1) deleted and to a poor prognosis of gastric cancer in humans. This is the first demonstration that bacterial infection can lead to apoptosis resistance and to cross-resistance to other inducers of apoptosis such as bacteria, chemotherapeutic agents, and radiation. The development of apoptosis resistance and downmodulation of p27(kip1) may contribute to the increased risk for gastric cancer observed in humans chronically exposed to H. pylori.

Indexed as

ApoptosisCell Cycle ProteinsHelicobacter pyloriTumor Suppressor ProteinsBacterial AdhesionCell CycleCell DivisionCell LineChronic DiseaseCyclin-Dependent Kinase Inhibitor p27Gastric MucosaGenes, p53Helicobacter InfectionsHumansMicrotubule-Associated ProteinsPhenotypeCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p27Microtubule-Associated ProteinsTumor Suppressor Proteins

Identifiers

PMID10948161
PMCPMC101795
OpenAlexW2125150113

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.