Evidence map›Paper›PMID 27540857›Full record

ArticleMolecular cell2016

Molecular Principles of Gene Fusion Mediated Rewiring of Protein Interaction Networks in Cancer.

Natasha S Latysheva, Matt E Oates, Louis Maddox, Tilman Flock, Julian Gough, Marija Buljan, Robert J Weatheritt, M Madan Babu

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed, 77 citations in OpenAlex.

  1. Whole-genome combinatorial gene fusions generate novel genes for advanced microbial trait development.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  17. A Dual Role for FADD in Human Precursor T-Cell Neoplasms.International journal of molecular sciences · 2022
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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 2 countries.

Natasha S LatyshevaMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. Electronic address: natashal@mrc-lmb.cam.ac.uk.
Matt E OatesDepartment of Computer Science, University of Bristol, Bristol BS8 1UB, UK.
Louis MaddoxMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Tilman FlockMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Julian GoughDepartment of Computer Science, University of Bristol, Bristol BS8 1UB, UK.
Marija BuljanMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Robert J WeatherittMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK; The Donnelly Centre, University of Toronto, Toronto, ON M5S 3E1, Canada.
M Madan BabuMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. Electronic address: madanm@mrc-lmb.cam.ac.uk.
MRC Laboratory of Molecular Biology · GBUniversity of Bristol · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G022771/1CIHRMedical Research Council MC-A025-5PK11-6801Medical Research Council MC_U105185859
6 · The paper itself

Abstract

Gene fusions are common cancer-causing mutations, but the molecular principles by which fusion protein products affect interaction networks and cause disease are not well understood. Here, we perform an integrative analysis of the structural, interactomic, and regulatory properties of thousands of putative fusion proteins. We demonstrate that genes that form fusions (i.e., parent genes) tend to be highly connected hub genes, whose protein products are enriched in structured and disordered interaction-mediating features. Fusion often results in the loss of these parental features and the depletion of regulatory sites such as post-translational modifications. Fusion products disproportionately connect proteins that did not previously interact in the protein interaction network. In this manner, fusion products can escape cellular regulation and constitutively rewire protein interaction networks. We suggest that the deregulation of central, interaction-prone proteins may represent a widespread mechanism by which fusion proteins alter the topology of cellular signaling pathways and promote cancer.

Indexed as

Gene FusionProtein Interaction MapsComputational BiologyDatabases, ProteinHumansNeoplasm ProteinsNeoplasmsProtein Interaction MappingProtein Processing, Post-TranslationalSignal TransductionTranscription FactorsUbiquitinationNeoplasm ProteinsTranscription Factorscancer genomicsfusion proteingene fusionprotein interaction networks

Identifiers

PMID27540857
PMCPMC5003813
OpenAlexW2511736040

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.