Evidence map›Paper›PMID 27897001›Full record

ArticlePacific Symposium on Biocomputing. Pacific Symposium on Biocomputing2017

DIFFERENTIAL PATHWAY DEPENDENCY DISCOVERY ASSOCIATED WITH DRUG RESPONSE ACROSS CANCER CELL LINES.

Gil Speyer, Divya Mahendra, Hai J Tran, Jeff Kiefer, Stuart L Schreiber, Paul A Clemons, Harshil Dhruv, Michael Berens, Seungchan Kim

Open access · goldAbstract read
In one paragraph

Article in Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
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

9 authors at 2 institutions in 1 country.

Gil SpeyerThe Translational Genomics Research Institute, Phoenix, AZ 85004, U.S.A., gspeyer@tgen.org.
Divya Mahendra
Hai J Tran
Jeff Kiefer
Stuart L Schreiber
Paul A Clemons
Harshil Dhruv
Michael Berens
Seungchan Kim
Translational Genomics Research Institute · USBroad Institute · US

Funding

Targeting vulnerabilities of therapy-resistant cancer cell states with small moleculesU01CA217848 · NCI · BROAD INSTITUTE, INC. · PI SCHREIBER, STUART L · 2017 to 2021
$5.8M
Cancer dependencies associated with genomic alterations and targeted by small molU01CA176152 · NCI · BROAD INSTITUTE, INC. · PI SCHREIBER, STUART L · 2013 to 2016
$4.4M
Systematic Development of Novel, Druggable Cancer TargetsU01CA168397 · NCI · TRANSLATIONAL GENOMICS RESEARCH INST · PI BERENS, MICHAEL E. · 2012 to 2016
$4.1M
NCI NIH HHS U01 CA168397NCI NIH HHS U01 CA176152NCI NIH HHS U01 CA217848
6 · The paper itself

Abstract

The effort to personalize treatment plans for cancer patients involves the identification of drug treatments that can effectively target the disease while minimizing the likelihood of adverse reactions. In this study, the gene-expression profile of 810 cancer cell lines and their response data to 368 small molecules from the Cancer Therapeutics Research Portal (CTRP) are analyzed to identify pathways with significant rewiring between genes, or differential gene dependency, between sensitive and non-sensitive cell lines. Identified pathways and their corresponding differential dependency networks are further analyzed to discover essentiality and specificity mediators of cell line response to drugs/compounds. For analysis we use the previously published method EDDY (Evaluation of Differential DependencY). EDDY first constructs likelihood distributions of gene-dependency networks, aided by known genegene interaction, for two given conditions, for example, sensitive cell lines vs. non-sensitive cell lines. These sets of networks yield a divergence value between two distributions of network likelihoods that can be assessed for significance using permutation tests. Resulting differential dependency networks are then further analyzed to identify genes, termed mediators, which may play important roles in biological signaling in certain cell lines that are sensitive or non-sensitive to the drugs. Establishing statistical correspondence between compounds and mediators can improve understanding of known gene dependencies associated with drug response while also discovering new dependencies. Millions of compute hours resulted in thousands of these statistical discoveries. EDDY identified 8,811 statistically significant pathways leading to 26,822 compound-pathway-mediator triplets. By incorporating STITCH and STRING databases, we could construct evidence networks for 14,415 compound-pathway-mediator triplets for support. The results of this analysis are presented in a searchable website to aid researchers in studying potential molecular mechanisms underlying cells' drug response as well as in designing experiments for the purpose of personalized treatment regimens.

Indexed as

AlgorithmsBenzenesulfonamidesCell Line, TumorComputational BiologyDeath-Associated Protein KinasesDrug Screening Assays, AntitumorGene Expression ProfilingGene Regulatory NetworksHigh-Throughput Screening AssaysHumansHypoxia-Inducible Factor 1, alpha SubunitNeoplasmsPrecision MedicineProtein Kinase InhibitorsPyrrolidinesSignal TransductionBenzenesulfonamidesDAPK3 protein, humanDeath-Associated Protein KinasesfedratinibHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitN-(3-chloro-7-indolyl)-1,4-benzenedisulphonamideProtein Kinase InhibitorsPyrrolidinesSulfonamides

Identifiers

PMID27897001
PMCPMC5180601
OpenAlexW2551883086

What OpenQuestion holds

Textmetadata
LicenceTDM
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.