Evidence map›Paper›PMID 31861467›Full record

ReviewCells2019

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors.

Pamela Bielli, Vittoria Pagliarini, Marco Pieraccioli, Cinzia Caggiano, Claudio Sette

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Non-Canonical Splicing and Its Implications in Brain Physiology and Cancer.International journal of molecular sciences · 2022
    Review
  12. Impacts and mechanisms of alternative mRNA splicing in cancer metabolism, immune response, and therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  13. Review
  14. Review
  15. New insights into the molecular genetics of recurrent malignant gliomas.Journal of molecular medicine (Berlin, Germany) · 2021
    Article
  16. Review
  17. Protein Arginine Methyltransferase 5 FunctionsFrontiers in cell and developmental biology · 2021
    Article
  18. Review
  19. Article
  20. Article
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 at 3 institutions in 1 country.

Pamela BielliDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.
Vittoria PagliariniDepartment of Neuroscience, Section of Human Anatomy, Catholic University of the Sacred Heart, 00168 Rome, Italy.
Marco PieraccioliLaboratory of Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy.
Cinzia CaggianoLaboratory of Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy.ORCID 0000-0002-2381-1848
Claudio SetteLaboratory of Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy.
Università Cattolica del Sacro Cuore · ITFondazione Santa Lucia · ITUniversity of Rome Tor Vergata · IT

Funding

Associazione Italiana per la Ricerca sul Cancro AIRC; IG18790Ministero della Salute RF-2016-02363460Ministero dell'Istruzione, dell'Università e della Ricerca MIUR; PRIN 2017Università Cattolica del Sacro Cuore Linea D1
6 · The paper itself

Abstract

Brain tumors are a heterogeneous group of neoplasms ranging from almost benign to highly aggressive phenotypes. The malignancy of these tumors mostly relies on gene expression reprogramming, which is frequently accompanied by the aberrant regulation of RNA processing mechanisms. In brain tumors, defects in alternative splicing result either from the dysregulation of expression and activity of splicing factors, or from mutations in the genes encoding splicing machinery components. Aberrant splicing regulation can generate dysfunctional proteins that lead to modification of fundamental physiological cellular processes, thus contributing to the development or progression of brain tumors. Herein, we summarize the current knowledge on splicing abnormalities in brain tumors and how these alterations contribute to the disease by sustaining proliferative signaling, escaping growth suppressors, or establishing a tumor microenvironment that fosters angiogenesis and intercellular communications. Lastly, we review recent efforts aimed at developing novel splicing-targeted cancer therapies, which employ oligonucleotide-based approaches or chemical modulators of alternative splicing that elicit an impact on brain tumor biology.

Indexed as

Alternative SplicingAnimalsBrain NeoplasmsCarcinogenesisDisease ProgressionGene Expression Regulation, NeoplasticHumansMutationOncogenesRNA SplicingRNA Splicing FactorsTumor MicroenvironmentRNA Splicing Factorsalternative splicingbrain tumorsEGFR signalinghippo signalingPRMT5splicing factorstumor microenvironment

Identifiers

PMID31861467
PMCPMC7016899
OpenAlexW2996632338

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.