Evidence map›Paper›PMID 36855776›Full record

ArticleClinical and translational medicine2023

Therapeutic potential of CDK11 in cancer.

Dalibor Blazek

Open access · goldAbstract readComment
In one paragraph

Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Targeting CDKs in the RNAPII transcription cycle.Nature reviews. Drug discovery · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Therapeutic potential of CDK11 in cancer.Clinical and translational medicine · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Dalibor BlazekCentral European Institute of Technology (CEITEC), Masaryk University, Brno, Czech Republic.ORCID https://orcid.org/0000-0003-4662-9982
Central European Institute of Technology · CZ

Funding

the Czech Science Foundation 21-19266Sthe Czech Science Foundation 23-04754X
6 · The paper itself

Abstract

Human cyclin-dependent kinases (CDKs) direct the progression of the cell cycle and transcription. They are deregulated in tumours, and despite their involvement in the regulation of basic cellular processes, many CDKs are promising targets for cancer therapy. CDK11 is an essential gene for the growth of many malignancies; however, its primary cellular function has been obscure, and the mode-of-action of OTS964, the first CDK11 inhibitor and antiproliferative compound, has been unknown. A recent study has shown that OTS964 prevents spliceosome activation, revealing a key role of CDK11 in the regulation of pre-mRNA splicing. In light of these findings, we discuss the therapeutic potential of CDK11 in cancer.

Indexed as

Cyclin-Dependent KinasesNeoplasmsCell CycleCell DivisionHumansRNA SplicingCDK19 protein, humanCyclin-Dependent KinasescancerCDK11OTS964pladienolide BSF3B1spliceosomesplicing

Identifiers

PMID36855776
PMCPMC9975460
OpenAlexW4322631842

What Socratic 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 Socratic graph.