Evidence map›Paper›PMID 21124949›Full record

ArticlePLoS computational biology2010

A computational approach to analyze the mechanism of action of the kinase inhibitor bafetinib.

Thomas R Burkard, Uwe Rix, Florian P Breitwieser, Giulio Superti-Furga, Jacques Colinge

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Vitexicarpin acts as a novel angiogenesis inhibitor and its target network.Evidence-based complementary and alternative medicine : eCAM · 2013
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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.

Thomas R BurkardResearch Center for Molecular Medicine of the Austrian Academy of Science, Vienna, Austria.
Uwe Rix
Florian P Breitwieser
Giulio Superti-Furga
Jacques Colinge
Austrian Academy of Sciences · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prediction of drug action in human cells is a major challenge in biomedical research. Additionally, there is strong interest in finding new applications for approved drugs and identifying potential side effects. We present a computational strategy to predict mechanisms, risks and potential new domains of drug treatment on the basis of target profiles acquired through chemical proteomics. Functional protein-protein interaction networks that share one biological function are constructed and their crosstalk with the drug is scored regarding function disruption. We apply this procedure to the target profile of the second-generation BCR-ABL inhibitor bafetinib which is in development for the treatment of imatinib-resistant chronic myeloid leukemia. Beside the well known effect on apoptosis, we propose potential treatment of lung cancer and IGF1R expressing blast crisis.

Indexed as

Models, BiologicalAntineoplastic AgentsApoptosisErbB ReceptorsHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Interaction Domains and MotifsProtein Interaction MappingProtein Kinase InhibitorsProteomicsPyrimidinesSignal TransductionAntineoplastic AgentsbafetinibEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsPyrimidines

Identifiers

PMID21124949
PMCPMC2987840
OpenAlexW2005506021

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.