Evidence map›Paper›PMID 19136474›Full record

ArticleCarcinogenesis2009

Phosphoaspirin (MDC-43), a novel benzyl ester of aspirin, inhibits the growth of human cancer cell lines more potently than aspirin: a redox-dependent effect.

Wenping Zhao, Gerardo G Mackenzie, Onika T Murray, Zhiquan Zhang, Basil Rigas

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
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  7. Article
  8. Phospho-Aspirin (MDC-22) Prevents Pancreatic Carcinogenesis in Mice.Cancer prevention research (Philadelphia, Pa.) · 2016
    Article
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  12. 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

5 authors at 1 institution in 1 country.

Wenping ZhaoDepartment of Medicine, Division of Cancer Prevention, Stony Brook University, Stony Brook, NY 11794-5200, USA.
Gerardo G Mackenzie
Onika T Murray
Zhiquan Zhang
Basil Rigas
Stony Brook University · US

Funding

No-Releasing Aspirin and Colon Cancer PreventionR01CA092423 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI RIGAS, BASIL · 2001 to 2011
$4.1M
Pancreatic Cancer Prevention with NO-releasing NSAIDsR01CA101019 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI RIGAS, BASIL · 2004 to 2008
$1.3M
NCI NIH HHS 2R01 CA92423NCI NIH HHS R01 CA092423NCI NIH HHS R01 CA101019
6 · The paper itself

Abstract

Aspirin is chemopreventive against colon and probably other cancers, but this effect is relatively weak and its chronic administration to humans is associated with significant side effects. Because of these limitations, extensive effort has been exerted to improve the pharmacological properties of aspirin. We have determined the anticancer activity and mechanisms of action of the novel para positional isomer of phosphoaspirin [P-ASA; MDC-43; 4-((diethoxyphosphoryloxy)methyl)phenyl 2-acetoxybenzoate]. P-ASA inhibited the growth of 10 human cancer cell lines originating from colon, lung, liver, pancreas and breast, at least 18- to 144-fold more potently than conventional aspirin. P-ASA achieved this effect by modulating cell kinetics; compared with controls, P-ASA reduced cell proliferation by up to 68%, increased apoptosis 5.5-fold and blocked cell cycle progression in the G(2)/M phase. P-ASA increased intracellular levels of reactive oxygen species (ROS), depleted glutathione levels and modulated cell signaling predominantly through the mitogen-activated protein kinase (p38 and c-jun N-terminal kinase), cyclooxygenase (COX) and nuclear factor-kappa B pathways. P-ASA targeted the mitochondria, increasing mitochondrial superoxide anion levels; this effect on ROS led to collapsed mitochondrial membrane potential and triggered the intrinsic apoptotic pathway. The antioxidant N-acetyl cysteine abrogated the cell growth inhibitory and signaling effects of P-ASA, underscoring the centrality of ROS in its mechanism of action. Our results, establishing P-ASA as a potent inhibitor of the growth of several human cancer cell lines, suggest that it may possess broad anticancer properties. We conclude that the novel P-ASA is a promising anticancer agent, which merits further evaluation.

Indexed as

AcetylcysteineAntineoplastic AgentsAntioxidantsApoptosisAspirinCell CycleCell DeathCell Line, TumorCell ProliferationHumansIsomerismMembrane Potential, MitochondrialOrganophosphatesOxidation-ReductionReactive Oxygen SpeciesSignal TransductionAcetylcysteineAntineoplastic AgentsAntioxidantsAspirinOrganophosphatesphosphoaspirinReactive Oxygen Species

Identifiers

PMID19136474
PMCPMC2650796
OpenAlexW2171757752

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.