Evidence map›Paper›PMID 26320181›Full record

ArticleOncotarget2015

A method for predicting target drug efficiency in cancer based on the analysis of signaling pathway activation.

Artem Artemov, Alexander Aliper, Michael Korzinkin, Ksenia Lezhnina, Leslie Jellen, Nikolay Zhukov, Sergey Roumiantsev, Nurshat Gaifullin, Alex Zhavoronkov, Nicolas Borisov and 1 more

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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

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  18. The expression of CCL18 in diffuse large B cell lymphoma and its mechanism research.Cancer biomarkers : section A of Disease markers · 2018
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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

11 authors at 5 institutions in 2 countries.

Artem ArtemovPathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR.
Alexander AliperD. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.
Michael KorzinkinPathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR.
Ksenia LezhninaPathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR.
Leslie JellenDepartment of Genetics, Genomics, and Informatics, University of Tennessee Health Science Center, Memphis, TN, USA.
Nikolay ZhukovD. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.
Sergey RoumiantsevD. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.
Nurshat GaifullinMoscow State University, Faculty of Fundamental Medicine, Moscow, Russia.
Alex ZhavoronkovInsilico Medicine, Inc., ETC, Johns Hopkins University, Baltimore, MD, USA.
Nicolas BorisovFirst Oncology Research and Advisory Center, Moscow, Russia.
Anton BuzdinPathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR.
Dmitry Rogachev National Research Center of Pediatric Hematology, Oncology and Immunology · RUJohns Hopkins University · USLomonosov Moscow State University · RUPirogov Russian National Research Medical University · RUUniversity of Tennessee Health Science Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A new generation of anticancer therapeutics called target drugs has quickly developed in the 21st century. These drugs are tailored to inhibit cancer cell growth, proliferation, and viability by specific interactions with one or a few target proteins. However, despite formally known molecular targets for every "target" drug, patient response to treatment remains largely individual and unpredictable. Choosing the most effective personalized treatment remains a major challenge in oncology and is still largely trial and error. Here we present a novel approach for predicting target drug efficacy based on the gene expression signature of the individual tumor sample(s). The enclosed bioinformatic algorithm detects activation of intracellular regulatory pathways in the tumor in comparison to the corresponding normal tissues. According to the nature of the molecular targets of a drug, it predicts whether the drug can prevent cancer growth and survival in each individual case by blocking the abnormally activated tumor-promoting pathways or by reinforcing internal tumor suppressor cascades. To validate the method, we compared the distribution of predicted drug efficacy scores for five drugs (Sorafenib, Bevacizumab, Cetuximab, Sorafenib, Imatinib, Sunitinib) and seven cancer types (Clear Cell Renal Cell Carcinoma, Colon cancer, Lung adenocarcinoma, non-Hodgkin Lymphoma, Thyroid cancer and Sarcoma) with the available clinical trials data for the respective cancer types and drugs. The percent of responders to a drug treatment correlated significantly (Pearson's correlation 0.77 p = 0.023) with the percent of tumors showing high drug scores calculated with the current algorithm.

Indexed as

Computational BiologyMolecular Targeted TherapyAlgorithmsAntineoplastic AgentsBiomarkers, TumorCell ProliferationCell SurvivalClinical Trials as TopicDatabases, GeneticDrug DiscoveryEnzyme ActivationGene Expression ProfilingGenetic Predisposition to DiseaseHumansNeoplasmsPatient SelectionAntineoplastic AgentsBiomarkers, TumorProtein Kinase InhibitorsProtein-Tyrosine Kinasesbioinformatic modelingcancerintracellular signaling pathwaypersonalized medicineresponse to target drug therapy

Identifiers

PMID26320181
PMCPMC4745731
OpenAlexW2168488626

What OpenQuestion holds

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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.