Evidence map›Paper›PMID 27197215›Full record

ArticleGenome research2016

Large-scale analysis of genome and transcriptome alterations in multiple tumors unveils novel cancer-relevant splicing networks.

Endre Sebestyén, Babita Singh, Belén Miñana, Amadís Pagès, Francesca Mateo, Miguel Angel Pujana, Juan Valcárcel, Eduardo Eyras

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Genome research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 186 papers.

0numbers the graph read from it
0cells of the map it votes in
186citing 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

186 citing papers in PubMed, 272 citations in OpenAlex.

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  19. MRAS: Master Regulator Analysis of Alternative Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. The RNA-Binding Proteins MCPIP2 and IGF2BP1 Competitively Modulate Breast Tumor Angiogenesis by Antagonizing VEGFA mRNA Stability and Expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article

126 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Endre SebestyénUniversitat Pompeu Fabra, E08003 Barcelona, Spain;
Babita SinghUniversitat Pompeu Fabra, E08003 Barcelona, Spain;
Belén MiñanaUniversitat Pompeu Fabra, E08003 Barcelona, Spain; Centre for Genomic Regulation, E08003 Barcelona, Spain;
Amadís PagèsUniversitat Pompeu Fabra, E08003 Barcelona, Spain;
Francesca MateoProgram Against Cancer Therapeutic Resistance (ProCURE), Catalan Institute of Oncology (ICO), Bellvitge Institute for Biomedical Research (IDIBELL), E08908 L'Hospitalet del Llobregat, Spain;
Miguel Angel PujanaProgram Against Cancer Therapeutic Resistance (ProCURE), Catalan Institute of Oncology (ICO), Bellvitge Institute for Biomedical Research (IDIBELL), E08908 L'Hospitalet del Llobregat, Spain;
Juan ValcárcelUniversitat Pompeu Fabra, E08003 Barcelona, Spain; Centre for Genomic Regulation, E08003 Barcelona, Spain; Catalan Institution for Research and Advanced Studies, E08010 Barcelona, Spain.
Eduardo EyrasUniversitat Pompeu Fabra, E08003 Barcelona, Spain; Catalan Institution for Research and Advanced Studies, E08010 Barcelona, Spain.
Universitat Pompeu Fabra · ESInstitució Catalana de Recerca i Estudis Avançats · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternative splicing is regulated by multiple RNA-binding proteins and influences the expression of most eukaryotic genes. However, the role of this process in human disease, and particularly in cancer, is only starting to be unveiled. We systematically analyzed mutation, copy number, and gene expression patterns of 1348 RNA-binding protein (RBP) genes in 11 solid tumor types, together with alternative splicing changes in these tumors and the enrichment of binding motifs in the alternatively spliced sequences. Our comprehensive study reveals widespread alterations in the expression of RBP genes, as well as novel mutations and copy number variations in association with multiple alternative splicing changes in cancer drivers and oncogenic pathways. Remarkably, the altered splicing patterns in several tumor types recapitulate those of undifferentiated cells. These patterns are predicted to be mainly controlled by MBNL1 and involve multiple cancer drivers, including the mitotic gene NUMA1 We show that NUMA1 alternative splicing induces enhanced cell proliferation and centrosome amplification in nontumorigenic mammary epithelial cells. Our study uncovers novel splicing networks that potentially contribute to cancer development and progression.

Indexed as

Alternative SplicingTranscriptomeAmino Acid MotifsBinding SitesCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticGenome, HumanHumansMutationNeoplasmsRNA Splicing FactorsRNA Splicing Factors

Identifiers

PMID27197215
PMCPMC4889968
OpenAlexW2338046461

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.