Evidence map›Paper›PMID 29373718›Full record

ArticleNeuro-oncology2018

The aberrant splicing of BAF45d links splicing regulation and transcription in glioblastoma.

Guillermo Aldave, Marisol Gonzalez-Huarriz, Angel Rubio, Juan Pablo Romero, Datta Ravi, Belén Miñana, Mar Cuadrado-Tejedor, Ana García-Osta, Roeland Verhaak, Enric Xipell and 17 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. PTBP1 and Cancer: From RNA Regulation to Therapeutic Potential.Journal of cellular and molecular medicine · 2025
    Review
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  10. PTBP1 is a Novel Poor Prognostic Factor for Glioma.BioMed research international · 2022
    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

27 authors at 10 institutions in 3 countries.

Guillermo AldaveDivision of Pediatric Neurosurgery, Department of Surgery, Texas Children's Hospital, Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, USA.
Marisol Gonzalez-HuarrizDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Angel RubioCEIT and TECNUN, University of Navarra, San Sebastian, Spain.
Juan Pablo RomeroCEIT and TECNUN, University of Navarra, San Sebastian, Spain.
Datta RaviCEIT and TECNUN, University of Navarra, San Sebastian, Spain.
Belén MiñanaCentre de Regulació Genòmica (CRG), Barcelona Institute of Science and Technology, Barcelona, Spain, Universitat Pompeu-Fabra, Barcelona, Spain.
Mar Cuadrado-TejedorHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Ana García-OstaHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Roeland VerhaakDepartment of Genomic Medicine, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Enric XipellDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Naiara Martinez-VélezDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Arlet Acanda de la RochaDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Montserrat PuigdellosesDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Marc García-MoureDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Miguel MarigilDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Jaime Gállego Pérez-LarrayaDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Oskar Marín-BejarHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Maite HuarteHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Maria Stella CarroDepartment of Neurosurgery (Neurocenter) Universitätsklinikum Freiburg, Freiburg, Germany.
Roberto FerrareseDepartment of Neurosurgery (Neurocenter) Universitätsklinikum Freiburg, Freiburg, Germany.
Cristobal Belda-IniestaFundación de Investigación HM Hospitales, Grupo HM, Spain.
Angel AyusoFundación de Investigación HM Hospitales, Grupo HM, Spain.
Ricardo Prat-AcínDepartment of Neurosurgery, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Fernando PastorHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Ricardo Díez-ValleHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Sonia TejadaHealth Research Institute of Navarra (IDISNA), Pamplona, Navarra, Spain.
Marta M AlonsoDepartment of Pediatrics, University Hospital of Navarra, Pamplona, Navarra, Spain.
Navarre Institute of Health Research · ESUniversidad de Navarra · ESUniversity Medical Center Freiburg · DECentro de Estudios e Investigaciones Técnicas de Gipuzkoa · ESHM Hospitales · ESHospital Universitari i Politècnic La Fe · ESPompeu Fabra University · ESTexas Children's Hospital · USThe University of Texas MD Anderson Cancer Center · USUniversidad San Pablo CEU · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Glioblastoma, the most aggressive primary brain tumor, is genetically heterogeneous. Alternative splicing (AS) plays a key role in numerous pathologies, including cancer. The objectives of our study were to determine whether aberrant AS could play a role in the malignant phenotype of glioma and to understand the mechanism underlying its aberrant regulation. Methods: We obtained surgical samples from patients with glioblastoma who underwent 5-aminolevulinic fluorescence-guided surgery. Biopsies were taken from the tumor center as well as from adjacent normal-appearing tissue. We used a global splicing array to identify candidate genes aberrantly spliced in these glioblastoma samples. Mechanistic and functional studies were performed to elucidate the role of our top candidate splice variant, BAF45d, in glioblastoma. Results: BAF45d is part of the switch/sucrose nonfermentable complex and plays a key role in the development of the CNS. The BAF45d/6A isoform is present in 85% of over 200 glioma samples that have been analyzed and contributes to the malignant glioma phenotype through the maintenance of an undifferentiated cellular state. We demonstrate that BAF45d splicing is mediated by polypyrimidine tract-binding protein 1 (PTBP1) and that BAF45d regulates PTBP1, uncovering a reciprocal interplay between RNA splicing regulation and transcription. Conclusions: Our data indicate that AS is a mechanism that contributes to the malignant phenotype of glioblastoma. Understanding the consequences of this biological process will uncover new therapeutic targets for this devastating disease.

Indexed as

Alternative SplicingGene Expression Regulation, NeoplasticBiomarkers, TumorBrain NeoplasmsCell MovementCell ProliferationDNA-Binding ProteinsGlioblastomaHeterogeneous-Nuclear RibonucleoproteinsHumansPolypyrimidine Tract-Binding ProteinProtein IsoformsTranscription FactorsTumor Cells, CulturedBiomarkers, TumorDNA-Binding ProteinsDPF2 protein, humanHeterogeneous-Nuclear RibonucleoproteinsPolypyrimidine Tract-Binding ProteinProtein IsoformsPTBP1 protein, humanTranscription Factors

Identifiers

PMID29373718
PMCPMC6007380
OpenAlexW2790197340

What OpenQuestion holds

Textmetadata
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Registered trials

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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.