Evidence map›Paper›PMID 32751160›Full record

ReviewCancers2020

The DYRK Family of Kinases in Cancer: Molecular Functions and Therapeutic Opportunities.

Jacopo Boni, Carlota Rubio-Perez, Nuria López-Bigas, Cristina Fillat, Susana de la Luna

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. RNA Splicing as a Therapeutic Target in Cancer.Annual review of pharmacology and toxicology · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. MyocardialAntioxidants (Basel, Switzerland) · 2025
    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.

Jacopo BoniCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology (BIST), Dr Aiguader 88, 08003 Barcelona, Spain.
Carlota Rubio-PerezCancer Science Programme, Institute for Research in Biomedicine (IRB), The Barcelona Institute of Science and Technology (BIST), Baldiri Reixac 10, 08028 Barcelona, Spain.ORCID 0000-0002-1921-168X
Nuria López-BigasCancer Science Programme, Institute for Research in Biomedicine (IRB), The Barcelona Institute of Science and Technology (BIST), Baldiri Reixac 10, 08028 Barcelona, Spain.
Cristina FillatCentro de Investigación Biomédica en Red en Enfermedades Raras (CIBERER), 28029 Madrid, Spain.
Susana de la LunaCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology (BIST), Dr Aiguader 88, 08003 Barcelona, Spain.ORCID 0000-0001-7765-916X
Centre for Biomedical Network Research on Rare Diseases · ESInstitució Catalana de Recerca i Estudis Avançats · ESInstitute for Research in Biomedicine · ES

Funding

Ministerio de Economía, Industria y Competitividad, Gobierno de España BES-2014-069983Ministerio de Economía, Industria y Competitividad, Gobierno de España BFU2016-76141-P
6 · The paper itself

Abstract

DYRK (dual-specificity tyrosine-regulated kinases) are an evolutionary conserved family of protein kinases with members from yeast to humans. In humans, DYRKs are pleiotropic factors that phosphorylate a broad set of proteins involved in many different cellular processes. These include factors that have been associated with all the hallmarks of cancer, from genomic instability to increased proliferation and resistance, programmed cell death, or signaling pathways whose dysfunction is relevant to tumor onset and progression. In accordance with an involvement of DYRK kinases in the regulation of tumorigenic processes, an increasing number of research studies have been published in recent years showing either alterations of DYRK gene expression in tumor samples and/or providing evidence of DYRK-dependent mechanisms that contribute to tumor initiation and/or progression. In the present article, we will review the current understanding of the role of DYRK family members in cancer initiation and progression, providing an overview of the small molecules that act as DYRK inhibitors and discussing the clinical implications and therapeutic opportunities currently available.

Indexed as

cell cyclecell survivalcellular signalingDYRK kinasesexpression dysregulationkinase inhibitorstumor progression

Identifiers

PMID32751160
PMCPMC7465136
OpenAlexW3045519314

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.