Evidence map›Paper›PMID 24874482›Full record

ReviewBritish journal of cancer2014

Molecular targets of aspirin and cancer prevention.

L Alfonso, G Ai, R C Spitale, G J Bhat

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

103 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Aspirin Reduces Plasma Concentrations of the Oncometabolite 2-Hydroxyglutarate: Results of a Randomized, Double-Blind, Crossover Trial.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016
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43 more citing papers are in PubMed but not listed here.

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

4 authors.

L AlfonsoDYouville College School of Pharmacy, Buffalo, NY, USA.
G AiDepartment of Pharmaceutical Sciences, South Dakota State University College of Pharmacy, Brookings, SD, USA.
R C SpitaleDepartment of Pharmaceutical Sciences, University of California, Irvine, CA, USA.
G J BhatDepartment of Pharmaceutical Sciences, South Dakota State University College of Pharmacy, Brookings, SD, USA.

Funding

p53 Acetylation as a Mechanism in Chemoprevention by AspirinR03CA133061 · NCI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI GUNAJE, JAYARAMA B · 2009 to 2010
$149k
NCI NIH HHS 5R03CA133061-02NCI NIH HHS R03 CA133061
6 · The paper itself

Abstract

Salicylates from plant sources have been used for centuries by different cultures to treat a variety of ailments such as inflammation, fever and pain. A chemical derivative of salicylic acid, aspirin, was synthesised and mass produced by the end of the 19th century and is one of the most widely used drugs in the world. Its cardioprotective properties are well established; however, recent evidence shows that it can also act as a chemopreventive agent. Its antithrombotic and anti-inflammatory actions occur through the inhibition of cyclooxygenases. The precise mechanisms leading to its anticancer effects are not clearly established, although multiple mechanisms affecting enzyme activity, transcription factors, cellular signalling and mitochondrial functions have been proposed. This review presents a brief account of the major COX-dependent and independent pathways described in connection with aspirin's anticancer effects. Aspirin's unique ability to acetylate biomolecules besides COX has not been thoroughly investigated nor have all the targets of its primary metabolite, salicylic acid been identified. Recent reports on the ability of aspirin to acetylate multiple cellular proteins warrant a comprehensive study to investigate the role of this posttranslational modification in its anticancer effects. In this review, we also raise the intriguing possibility that aspirin may interact and acetylate cellular molecules such as RNA, and metabolites such as CoA, leading to a change in their function. Research in this area will provide a greater understanding of the mechanisms of action of this drug.

Indexed as

Anticarcinogenic AgentsAnti-Inflammatory Agents, Non-SteroidalAspirinHumansMolecular Targeted TherapyNeoplasmsAnticarcinogenic AgentsAnti-Inflammatory Agents, Non-SteroidalAspirin

Identifiers

PMID24874482
PMCPMC4090734

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.