Evidence map›Paper›PMID 28208660›Full record

ReviewInternational journal of molecular sciences2017

Splice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy.

Cherine Abou-Fayçal, Anne-Sophie Hatat, Sylvie Gazzeri, Beatrice Eymin

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Receptor tyrosine kinase inhibitors in cancer.Cellular and molecular life sciences : CMLS · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Splicing factor SRSF2-centric gene regulation.International journal of biological sciences · 2021
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Hypoxia-induced alternative splicing: the 11th Hallmark of Cancer.Journal of experimental & clinical cancer research : CR · 2020
    Review
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

4 authors.

Cherine Abou-FayçalTeam RNA Splicing, Cell Signaling and Response to Therapies, Institute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, University Grenoble Alpes, Grenoble 38702, France. cherineaf@gmail.com.
Anne-Sophie HatatTeam RNA Splicing, Cell Signaling and Response to Therapies, Institute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, University Grenoble Alpes, Grenoble 38702, France. anne-sophie.hatat@univ-grenoble-alpes.fr.
Sylvie GazzeriTeam RNA Splicing, Cell Signaling and Response to Therapies, Institute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, University Grenoble Alpes, Grenoble 38702, France. sylvie.gazzeri@univ-grenoble-alpes.fr.
Beatrice EyminTeam RNA Splicing, Cell Signaling and Response to Therapies, Institute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, University Grenoble Alpes, Grenoble 38702, France. beatrice.eymin@univ-grenoble-alpes.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Receptor tyrosine kinases (RTKs) belong to a family of transmembrane receptors that display tyrosine kinase activity and trigger the activation of downstream signalling pathways mainly involved in cell proliferation and survival. RTK amplification or somatic mutations leading to their constitutive activation and oncogenic properties have been reported in various tumour types. Numerous RTK-targeted therapies have been developed to counteract this hyperactivation. Alternative splicing of pre-mRNA has recently emerged as an important contributor to cancer development and tumour maintenance. Interestingly, RTKs are alternatively spliced. However, the biological functions of RTK splice variants, as well as the upstream signals that control their expression in tumours, remain to be understood. More importantly, it remains to be determined whether, and how, these splicing events may affect the response of tumour cells to RTK-targeted therapies, and inversely, whether these therapies may impact these splicing events. In this review, we will discuss the role of alternative splicing of RTKs in tumour progression and response to therapies, with a special focus on two major RTKs that control proliferation, survival, and angiogenesis, namely, epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor-1 (VEGFR1).

Indexed as

Alternative SplicingMultigene FamilyAngiogenesis InhibitorsBiomarkersDisease ProgressionErbB ReceptorsGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyNeoplasmsPrognosisProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesRNA PrecursorsVascular Endothelial Growth Factor Receptor-1Angiogenesis InhibitorsBiomarkersErbB ReceptorsProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesRNA PrecursorsVascular Endothelial Growth Factor Receptor-1alternative splicingangiogenesiscancerEGFRreceptor tyrosine kinasestargeted therapiestumourigenesisVEGFR

Identifiers

PMID28208660
PMCPMC5343918

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.