Evidence map›Paper›PMID 38072949›Full record

ArticleScientific reports2023

Theoretical basis validation and oxidative stress markers for cancer prevention clinical trials of aspirin.

Takahiro Hamoya, Susumu Tomono, Shingo Miyamoto, Gen Fujii, Keiji Wakabayashi, Michihiro Mutoh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Targeting G6PD with Benzimidazole and Thiazole Derivatives SuppressesInternational journal of molecular sciences · 2025
    Article
  2. Review
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

6 authors at 3 institutions in 1 country.

Takahiro HamoyaDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Susumu TomonoDepartment of Microbiology and Immunology, Aichi Medical University, Nagakute, Aichi, 480-1195, Japan.
Shingo MiyamotoDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Gen FujiiDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Keiji WakabayashiGraduate Division of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan.
Michihiro MutohDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan. mimutoh@koto.kpu-m.ac.jp.
Kyoto Prefectural University of Medicine · JPAichi Medical University · JPUniversity of Shizuoka · JP

Funding

Japan Agency for Medical Research and Development 23ck0106806h0001
6 · The paper itself

Abstract

Aspirin, a nonsteroidal anti-inflammatory drug, has been proven effective in a clinical trial of carcinogenesis blockade. However, various modes of action have been reported for these effects. Thus, in this study, we aimed to present reasonable mode of actions as a proof of concept for human trials, especially trials for patients with familial adenomatous polyposis (FAP). Aspirin treatment at 1000 ppm inhibited intestinal tumorigenesis in FAP model Min mice. As a mode of action, aspirin regulated β-catenin signaling, inflammation, and oxidative stress both in vivo and in vitro. Furthermore, we examined novel markers predictive of aspirin treatment based on liquid biopsy. Here, we demonstrated that aspirin reduced the levels of reactive carbonyl species in the serum of Min mice. These data are expected to be of use for proof of concept of aspirin human trials and implied for the prediction of aspirin efficacy.

Indexed as

Adenomatous Polyposis ColiAspirinAnimalsAnti-Inflammatory Agents, Non-SteroidalHumansInflammationMiceOxidative StressAnti-Inflammatory Agents, Non-SteroidalAspirin

Identifiers

PMID38072949
PMCPMC10711014
OpenAlexW4389555944

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.