Evidence map›Paper›PMID 27528223›Full record

ArticleOncotarget2016

Suppressed Helicobacter pylori-associated gastric tumorigenesis in Fat-1 transgenic mice producing endogenous ω-3 polyunsaturated fatty acids.

Young-Min Han, Kyung-Jo Kim, Migyeung Jeong, Jong-Min Park, Eun-Jin Go, Jing X Kang, Sung Pyo Hong, Ki Baik Hahm

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 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
1.6field-weighted citation impact, top 16% 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, 17 citations in OpenAlex.

  1. Article
  2. Transcriptome profiling analysis of the response to walnut polyphenol extract inJournal of clinical biochemistry and nutrition · 2021
    Article
  3. Article
  4. Dietary intake of walnut preventedJournal of clinical biochemistry and nutrition · 2021
    Article
  5. Rejuvenation ofFrontiers in pharmacology · 2021
    Article
  6. Walnut polyphenol extracts inhibitJournal of clinical biochemistry and nutrition · 2020
    Article
  7. Review
  8. Article
  9. 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 2 countries.

Young-Min HanCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, Korea.
Kyung-Jo KimDepartment of Gastroenterology, University of Ulsan, Seoul Asan Medical Center, Seoul, Korea.
Migyeung JeongCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, Korea.
Jong-Min ParkCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, Korea.
Eun-Jin GoCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, Korea.
Jing X KangLaboratory for Lipid Medicine and Technology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Sung Pyo HongDepartment of Gastroenterology, CHA Bundang Medical Center, Seongnam, Korea.
Ki Baik HahmCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, Korea.
CHA University · KRAsan Medical Center · KRCHA University Bundang Medical Center · KRMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dietary approaches to preventing Helicobacter pylori (H. pylori)-associated gastric carcinogenesis are widely accepted because surrounding break-up mechanisms are mandatory for cancer prevention, however, eradication alone has been proven to be insufficient. Among these dietary interventions, omega-3-polyunsaturated-fatty acids (ω-3 PUFAs) are often the first candidate selected. However, there was no trial of fatty acids in preventing H. pylori-associated carcinogenesis and inconclusive results have been reported, likely based on inconsistent dietary administration. In this study, we developed an H. pylori initiated-, high salt diet promoted-gastric tumorigenesis model and conducted a comparison between wild-type (WT) and Fat-1-transgenic (TG)-mice. Gross and pathological lesions in mouse stomachs were evaluated at 16, 24, 32, and 45 weeks after H. pylori infection, and the underlying molecular changes to explain the cancer preventive effects were investigated. Significant changes in: i) ameliorated gastric inflammations at 16 weeks of H. pylori infection, ii) decreased angiogenic growth factors at 24 weeks, iii) attenuated atrophic gastritis and tumorigenesis at 32 weeks, and iv) decreased gastric cancer at 45 weeks were all noted in Fat-1-TG-mice compared to WT-mice. While an increase in the expression of Cyclooxygenase (COX)-2, and reduced expression of the tumor suppressive 15-PGDH were observed in WT-mice throughout the experimental periods, the expression of Hydroxyprostaglandin dehydrogenase (15-PGDH) was preserved in Fat-1-TG-mice. Using a comparative protein array, attenuated expressions of proteins implicated in proliferation and inflammation were observed in Fat-1-TG-mice compared to WT-mice. Conclusively, long-term administration of ω-3 PUFAs can suppress H. pylori-induced gastric tumorigenesis through a dampening of inflammation and reduced proliferation in accordance with afforded rejuvenation.

Indexed as

AnimalsCadherinsCarcinogenesisFatty Acids, Omega-3Helicobacter InfectionsHelicobacter pyloriInflammationMiceMice, TransgenicStomach NeoplasmsCadherinsfat1 protein, mouseFatty Acids, Omega-315-PGDHanti-proliferationCOX-2Fat-1 transgenic miceω-3 PUFAs

Identifiers

PMID27528223
PMCPMC5341824
OpenAlexW2516425879

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.