Evidence map›Paper›PMID 26438695›Full record

ArticleDisease models & mechanisms2015

From drug response profiling to target addiction scoring in cancer cell models.

Bhagwan Yadav, Peddinti Gopalacharyulu, Tea Pemovska, Suleiman A Khan, Agnieszka Szwajda, Jing Tang, Krister Wennerberg, Tero Aittokallio

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Bhagwan YadavInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Peddinti GopalacharyuluInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Tea PemovskaInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Suleiman A KhanInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Agnieszka SzwajdaInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Jing TangInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Krister WennerbergInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland.
Tero AittokallioInstitute for Molecular Medicine Finland (FIMM), Nordic EMBL Partnership for Molecular Medicine, University of Helsinki, FI-00014 Helsinki, Finland tero.aittokallio@fimm.fi.
University of Helsinki · FIInstitute for Molecular Medicine Finland · FI

Funding

Wellcome Trust
6 · The paper itself

Abstract

Deconvoluting the molecular target signals behind observed drug response phenotypes is an important part of phenotype-based drug discovery and repurposing efforts. We demonstrate here how our network-based deconvolution approach, named target addiction score (TAS), provides insights into the functional importance of druggable protein targets in cell-based drug sensitivity testing experiments. Using cancer cell line profiling data sets, we constructed a functional classification across 107 cancer cell models, based on their common and unique target addiction signatures. The pan-cancer addiction correlations could not be explained by the tissue of origin, and only correlated in part with molecular and genomic signatures of the heterogeneous cancer cells. The TAS-based cancer cell classification was also shown to be robust to drug response data resampling, as well as predictive of the transcriptomic patterns in an independent set of cancer cells that shared similar addiction signatures with the 107 cancers. The critical protein targets identified by the integrated approach were also shown to have clinically relevant mutation frequencies in patients with various cancer subtypes, including not only well-established pan-cancer genes, such as PTEN tumor suppressor, but also a number of targets that are less frequently mutated in specific cancer types, including ABL1 oncoprotein in acute myeloid leukemia. An application to leukemia patient primary cell models demonstrated how the target deconvolution approach offers functional insights into patient-specific addiction patterns, such as those indicative of their receptor-type tyrosine-protein kinase FLT3 internal tandem duplication (FLT3-ITD) status and co-addiction partners, which may lead to clinically actionable, personalized drug treatment developments. To promote its application to the future drug testing studies, we have made available an open-source implementation of the TAS calculation in the form of a stand-alone R package.

Indexed as

Drug Delivery SystemsModels, BiologicalAntineoplastic AgentsCell Line, TumorGene Expression ProfilingHumansLeukemiaOrgan SpecificityAntineoplastic AgentsCell-based drug sensitivity profilingDrug-target addiction scoringExperimental-computational target deconvolutionPan-cancer modelingPersonalized cancer medicine

Identifiers

PMID26438695
PMCPMC4610238
OpenAlexW2158396858

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.