Evidence map›Paper›PMID 15188000›Full record

ArticleBritish journal of cancer2004

Evidence for colorectal cancer cell specificity of aspirin effects on NF kappa B signalling and apoptosis.

F V N Din, M G Dunlop, L A Stark

Open access · hybridAbstract readComparative Study
In one paragraph

Article in British journal of cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  12. Effect of aspirin use on gastric cancer incidence and survival: A systematic review and meta-analysis.JGH open : an open access journal of gastroenterology and hepatology · 2020
    Article
  13. Article
  14. Aspirin suppresses tumor cell-induced angiogenesis and their incongruity.Journal of cell communication and signaling · 2019
    Article
  15. 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

3 authors at 3 institutions in 2 countries.

F V N DinColon Cancer Genetics Group, University of Edinburgh Department of Oncology and MRC Human Genetics Unit, Western General Hospital, Crewe Rd, Edinburgh EH4 2XU, Scotland.
M G Dunlop
L A Stark
Cancer Genetics (United States) · USEdinburgh Cancer Research · GBWestern General Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiological evidence indicates that non-steroidal anti-inflammatory drugs (NSAIDs) protect against colorectal cancer (CRC) to a greater degree than other non-gastrointestinal cancers, but the molecular basis for this difference is unknown. We previously reported that aspirin induces signal-specific I kappa B alpha degradation followed by NF kappa B nuclear translocation in CRC cells, and that this mechanism contributes substantially to aspirin-induced apoptosis. Here, we explored the hypothesis that cell-type specific effects on NF kappa B signalling are responsible for the observed differences in protection by aspirin against CRC compared to breast and gynaecological cancers. We also assessed whether COX-2 expression, mutation status of adenomatous polyposis coli (APC), beta-catenin, p53, or DNA mismatch repair (MMR) genes in CRC lines influenced aspirin-induced effects. We found that aspirin induced concentration-dependent I kappa B alpha degradation, NF kappa B nuclear translocation and apoptosis in all CRC lines studied. However, there was no such effect on the other cancer cell types, indicating a considerable degree of cell-type specificity. The lack of effect on NF kappa B signalling, paralleled by absence of an apoptotic response to aspirin in non-CRC lines, strongly suggests a molecular rationale for the particular protective effect of NSAIDs against CRC. Effects on NF kappa B and apoptosis were observed irrespective of COX-2 expression, or mutation status in APC, beta-catenin, p53 and DNA MMR genes, underscoring the generality of the aspirin effect on NF kappa B in CRC cells. These findings raise the possibility of cell-type specific targets for the development of novel chemopreventive agents.

Indexed as

Adenomatous Polyposis ColiApoptosisAspirinbeta CateninBreast NeoplasmsCell NucleusColorectal NeoplasmsCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsCytoskeletal ProteinsDNA RepairEndometrial NeoplasmsFemaleHumansI-kappa B ProteinsAspirinbeta CateninCTNNB1 protein, humanCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsCytoskeletal ProteinsI-kappa B ProteinsIsoenzymesMembrane ProteinsNF-kappa BProstaglandin-Endoperoxide SynthasesPTGS2 protein, humanTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID15188000
PMCPMC2409803
OpenAlexW2060533030

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.