Evidence map›Paper›PMID 16103895›Full record

ArticleThe pharmacogenomics journal2005

Linking pathway gene expressions to the growth inhibition response from the National Cancer Institute's anticancer screen and drug mechanism of action.

R Huang, A Wallqvist, N Thanki, D G Covell

Abstract readValidation Study
PubMed Publisher
In one paragraph

Article in The pharmacogenomics journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  6. Integrating systems biology sources illuminates drug action.Clinical pharmacology and therapeutics · 2014
    Article
  7. Pathway analysis for drug repositioning based on public database mining.Journal of chemical information and modeling · 2014
    Article
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  12. Large-scale elucidation of drug response pathways in humans.Journal of computational biology : a journal of computational molecular cell biology · 2012
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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

4 authors at 3 institutions in 1 country.

R HuangDevelopmental Therapeutics Program, Screening Technologies Branch, Laboratory of Computational Technologies, National Cancer Institute-Frederick, Frederick, MD 21702, USA.
A Wallqvist
N Thanki
D G Covell
Science Applications International Corporation (United States) · USFrederick National Laboratory for Cancer Research · USNational Cancer Institute · US

Funding

PHS HHS N01 C0 12400
6 · The paper itself

Abstract

Novel strategies are proposed to quantitatively analyze and relate biological pathways to drug responses using gene expression and small-molecule growth inhibition data (GI(50)) derived from the National Cancer Institute's 60 cancer cells (NCI(60)). We have annotated groups of drug GI(50) responses with pathways defined by the Kyoto Encyclopedia of Genes and Genomes (KEGG) and BioCarta, and functional categories defined by Gene Ontology (GO), through correlations between pathway gene expression patterns and drug GI(50) profiles. Drug-gene-pathway relationships may then be utilized to find drug targets or target-specific drugs. Significantly correlated pathways and the gene products involved represent interesting targets for further exploration, whereas drugs that are significantly correlated with only certain pathways are more likely to be target specific. Separate pathway clustering finds that pathways engaged in the same biological process tend to have similar drug correlation patterns. The biological and statistical significances of our method are established by comparison to known small-molecule inhibitor-gene target relationships reported in the literature and by standard randomization procedures. The results of our pathway, gene expression and drug-induced growth inhibition associations, can serve as a basis for proposing testable hypotheses about potential anticancer drugs, their targets, and mechanisms of action.

Indexed as

Databases, FactualDatabases, GeneticDrug Screening Assays, AntitumorGene Expression ProfilingGene Expression Regulation, NeoplasticAntineoplastic AgentsDrug Resistance, NeoplasmHumansInformation Storage and RetrievalLethal Dose 50National Institutes of Health (U.S.)NeoplasmsPredictive Value of TestsTumor Cells, CulturedUnited StatesAntineoplastic Agents

Identifiers

PMID16103895
OpenAlexW1995487754

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.