Evidence map›Paper›PMID 26988076›Full record

ArticleScientific reports2016

Identification of Potential Drug Targets in Cancer Signaling Pathways using Stochastic Logical Models.

Peican Zhu, Hamidreza Montazeri Aliabadi, Hasan Uludağ, Jie Han

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  7. International journal of molecular sciences · 2018
    Article
  8. Article
  9. Boolean network modeling in systems pharmacology.Journal of pharmacokinetics and pharmacodynamics · 2018
    Review
  10. Article
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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 2 institutions in 2 countries.

Peican ZhuDepartment of Electrical and Computer Engineering, University of Alberta, Edmonton, AB T6G 1H9, Canada.
Hamidreza Montazeri AliabadiSchool of Pharmacy, Chapman University, Irvine, CA 92618, USA.
Hasan UludağDepartment of Chemical and Material Engineering, University of Alberta, Edmonton, AB T6G 1H9, Canada.
Jie HanDepartment of Electrical and Computer Engineering, University of Alberta, Edmonton, AB T6G 1H9, Canada.
University of Alberta · CAChapman University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The investigation of vulnerable components in a signaling pathway can contribute to development of drug therapy addressing aberrations in that pathway. Here, an original signaling pathway is derived from the published literature on breast cancer models. New stochastic logical models are then developed to analyze the vulnerability of the components in multiple signalling sub-pathways involved in this signaling cascade. The computational results are consistent with the experimental results, where the selected proteins were silenced using specific siRNAs and the viability of the cells were analyzed 72 hours after silencing. The genes elF4E and NFkB are found to have nearly no effect on the relative cell viability and the genes JAK2, Stat3, S6K, JUN, FOS, Myc, and Mcl1 are effective candidates to influence the relative cell growth. The vulnerabilities of some targets such as Myc and S6K are found to vary significantly depending on the weights of the sub-pathways; this will be indicative of the chosen target to require customization for therapy. When these targets are utilized, the response of breast cancers from different patients will be highly variable because of the known heterogeneities in signaling pathways among the patients. The targets whose vulnerabilities are invariably high might be more universally acceptable targets.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalComputational BiologyFemaleGene Expression Regulation, NeoplasticHumansRNA, Small InterferingSignal TransductionStochastic ProcessesAntineoplastic AgentsRNA, Small Interfering

Identifiers

PMID26988076
PMCPMC4796823
OpenAlexW2305802361

What OpenQuestion holds

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LicenceCC BY
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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.