Evidence map›Paper›PMID 26513174›Full record

ArticleOncotarget2015

MDP, a database linking drug response data to genomic information, identifies dasatinib and statins as a combinatorial strategy to inhibit YAP/TAZ in cancer cells.

Cristian Taccioli, Giovanni Sorrentino, Alessandro Zannini, Jimmy Caroli, Domenico Beneventano, Laura Anderlucci, Marco Lolli, Silvio Bicciato, Giannino Del Sal

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  7. Drug repurposing for cancer therapy.Signal transduction and targeted therapy · 2024
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  13. Statins: a repurposed drug to fight cancer.Journal of experimental & clinical cancer research : CR · 2021
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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

9 authors at 4 institutions in 1 country.

Cristian TaccioliDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena 41125, Italy.
Giovanni SorrentinoLaboratorio Nazionale CIB (LNCIB), Area Science Park, Trieste 34149, Italy.
Alessandro ZanniniLaboratorio Nazionale CIB (LNCIB), Area Science Park, Trieste 34149, Italy.
Jimmy CaroliDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena 41125, Italy.
Domenico BeneventanoDipartimento di Ingegneria "Enzo Ferrari", Modena 41125, Italy.
Laura AnderlucciDipartimento di Scienze Statistiche, Bologna 40124, Italy.
Marco LolliDepartment of Science and Drug Technology, University of Torino, Torino 10125, Italy.
Silvio BicciatoDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena 41125, Italy.
Giannino Del SalLaboratorio Nazionale CIB (LNCIB), Area Science Park, Trieste 34149, Italy.
University of Modena and Reggio Emilia · ITUniversity of Trieste · ITFerrari (Italy) · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted anticancer therapies represent the most effective pharmacological strategies in terms of clinical responses. In this context, genetic alteration of several oncogenes represents an optimal predictor of response to targeted therapy. Integration of large-scale molecular and pharmacological data from cancer cell lines promises to be effective in the discovery of new genetic markers of drug sensitivity and of clinically relevant anticancer compounds. To define novel pharmacogenomic dependencies in cancer, we created the Mutations and Drugs Portal (MDP, http://mdp.unimore.it), a web accessible database that combines the cell-based NCI60 screening of more than 50,000 compounds with genomic data extracted from the Cancer Cell Line Encyclopedia and the NCI60 DTP projects. MDP can be queried for drugs active in cancer cell lines carrying mutations in specific cancer genes or for genetic markers associated to sensitivity or resistance to a given compound. As proof of performance, we interrogated MDP to identify both known and novel pharmacogenomics associations and unveiled an unpredicted combination of two FDA-approved compounds, namely statins and Dasatinib, as an effective strategy to potently inhibit YAP/TAZ in cancer cells.

Indexed as

Databases, GeneticDatabases, PharmaceuticalAcyltransferasesAdaptor Proteins, Signal TransducingAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorDasatinibHT29 CellsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsPharmacogeneticsPhosphoproteinsSignal TransductionTranscription FactorsYAP-Signaling ProteinsAcyltransferasesAdaptor Proteins, Signal TransducingDasatinibHydroxymethylglutaryl-CoA Reductase InhibitorsPhosphoproteinsTAFAZZIN protein, humanTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinscancerHippo pathwaypharmacogenomicssmall moleculestargeted therapy

Identifiers

PMID26513174
PMCPMC4770742
OpenAlexW2173710913

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.