Evidence map›Paper›PMID 25714784›Full record

ArticleEuropean journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)2016

The protein kinase promiscuities in the cancer-preventive mechanisms of NSAIDs.

Povilas Norvaisas, Diana Chan, Kenji Yokoi, Bhuvanesh Dave, Arturas Ziemys

Abstract read
In one paragraph

Article in European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 95% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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.

Povilas NorvaisasThe Houston Methodist Research Institute, Houston, Texas, USA.
Diana Chan
Kenji Yokoi
Bhuvanesh Dave
Arturas Ziemys
Houston Methodist · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NSAIDs have been observed to have cancer-preventive properties, but the actual mechanism is elusive. We hypothesize that NSAIDs might have an effect through common pathways and targets of anticancer drugs by exploiting promiscuities of anticancer drug targets. Here, we have explored NSAIDs by their structural and pharmacophoric similarities with small anticancer molecules. In-silico analyses have shown a strong similarity between NSAIDs and protein kinase (PK) inhibitors. The calculated affinities of NSAIDs were found to be lower than the affinities of anticancer drugs, but higher than the affinities of compounds that are not specific to PKs. The competitive inhibition model suggests that PK might be inhibited by around 10%, which was confirmed by biochemical screening of some NSAIDs against PKs. NSAIDs did not affect all PKs universally, but had specificities for certain sets of PKs, which differed according to the NSAID. The study revealed potentially new features and mechanisms of NSAIDs that are useful in explaining their role in cancer prevention, which might lead to clinically significant breakthroughs in the future.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalAntineoplastic AgentsBinding, CompetitiveHumansNeoplasmsProtein Kinase InhibitorsProtein KinasesAnti-Inflammatory Agents, Non-SteroidalAntineoplastic AgentsProtein Kinase InhibitorsProtein Kinases

Identifiers

PMID25714784
PMCPMC4885542
OpenAlexW2086233614

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.