Evidence map›Paper›PMID 27499580›Full record

ArticleJournal of clinical biochemistry and nutrition2016

The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer.

Noriko Nakajima, Karina Kozu, Shun Kobayashi, Ryu Nishiyama, Rie Okubo, Yuichi Akai, Mitsuhiko Moriyama, Noriko Kinukawa

Open access · diamondAbstract read
In one paragraph

Article in Journal of clinical biochemistry and nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Effect ofImmunotherapy · 2025
    Review
  2. Impact of Helicobacter pylori Infection and Treatment on Colorectal Cancer in a Large, Nationwide Cohort.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
    Article
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  6. Review
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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 1 institution in 1 country.

Noriko NakajimaDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Karina KozuDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Shun KobayashiDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Ryu NishiyamaDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Rie OkuboDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Yuichi AkaiDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Mitsuhiko MoriyamaDepartment of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Noriko KinukawaDepartment of Pathology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of IGF-1R has been demonstrated in gastrointestinal cancers, and its expression is reported as the result of the loss of tumor suppressors. IL-16 is involved in the pathophysiological process of chronic inflammatory diseases. The aim of this study is to determine the changes in the expression of IGF-1R in intestinal metaplasia (IM) and gastric cancer (GC) as well as the effect of Helicobacter pylori (H. pylori) and IL-16 on cell proliferation and IGF-1R expression in gastric cells. AGS cells were incubated with combinations of IL-16 and H. pylori. Gastric cell proliferation was studied by BrdU uptake. In H. pylori infected mucosa, IGF-1R was significantly higher in IM than chronic gastritis (CG), and also higher in GC than CG and IM. H. pylori significantly decreased BrdU uptake. IL-16 increased BrdU uptake and IGF-1R on AGS cells which had been decreased by H. pylori. Co-incubation with IL-16 increased the expression of IGF-1R mRNA in H. pylori infected cells. We conclude that the expression of IGF-1R in H. pylori infected gastric mucosa may indicate an early stage of carcinogenesis. The IL-16 secretion by H. pylori can be a trigger for the expression of IGF-1R, and it may also be a factor for gastric carcinogenesis.

Indexed as

chronic gastritisgastric cancerHelicobacter pyloriIGF-1Rintestinal metaplasia

Identifiers

PMID27499580
PMCPMC4933692
OpenAlexW2398791624

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.