Evidence map›Paper›PMID 25919796›Full record

ArticleScientific reports2015

Increased signaling entropy in cancer requires the scale-free property of protein interaction networks.

Andrew E Teschendorff, Christopher R S Banerji, Simone Severini, Reimer Kuehn, Peter Sollich

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

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  5. Statistical mechanics meets single-cell biology.Nature reviews. Genetics · 2021
    Review
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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

5 authors.

Andrew E Teschendorff1] Statistical Cancer Genomics, Paul O'Gorman Building, UCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6BT, United Kingdom [2] CAS Key Lab for Computational Biology, CAS-MPG Partner Institute for Computational Biology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China.
Christopher R S Banerji1] Statistical Cancer Genomics, Paul O'Gorman Building, UCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6BT, United Kingdom [2] Centre for Mathematics and Physics in the Life Sciences and Experimental Biology, University College London, London WC1E6BT United Kingdom [3] Department of Computer Science, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Simone SeveriniDepartment of Computer Science, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Reimer KuehnDepartment of Mathematics, King's College London, London WC2R 2LS, UK.
Peter SollichDepartment of Mathematics, King's College London, London WC2R 2LS, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the key characteristics of cancer cells is an increased phenotypic plasticity, driven by underlying genetic and epigenetic perturbations. However, at a systems-level it is unclear how these perturbations give rise to the observed increased plasticity. Elucidating such systems-level principles is key for an improved understanding of cancer. Recently, it has been shown that signaling entropy, an overall measure of signaling pathway promiscuity, and computable from integrating a sample's gene expression profile with a protein interaction network, correlates with phenotypic plasticity and is increased in cancer compared to normal tissue. Here we develop a computational framework for studying the effects of network perturbations on signaling entropy. We demonstrate that the increased signaling entropy of cancer is driven by two factors: (i) the scale-free (or near scale-free) topology of the interaction network, and (ii) a subtle positive correlation between differential gene expression and node connectivity. Indeed, we show that if protein interaction networks were random graphs, described by Poisson degree distributions, that cancer would generally not exhibit an increased signaling entropy. In summary, this work exposes a deep connection between cancer, signaling entropy and interaction network topology.

Indexed as

AlgorithmsDatabases, GeneticEntropyHumansModels, BiologicalNeoplasmsPoisson DistributionProtein Interaction MapsSignal TransductionTranscriptome

Identifiers

PMID25919796
PMCPMC4412078

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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.