Evidence map›Paper›PMID 20671765›Full record

ReviewNature reviews. Drug discovery2010

Multifaceted polo-like kinases: drug targets and antitargets for cancer therapy.

Klaus Strebhardt

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Drug discovery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 359 papers.

0numbers the graph read from it
0cells of the map it votes in
359citing papers in PubMed
19.8field-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

359 citing papers in PubMed, 646 citations in OpenAlex.

  1. Review
  2. Article
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  6. Review
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  8. Mass Spectrometry for Proteomics-Based Investigation.Advances in experimental medicine and biology · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. GSK461364 Inhibits NLRP3 Inflammasome by Targeting NEK7 Phosphorylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

299 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Klaus StrebhardtDepartment of Obstetrics and Gynaecology, School of Medicine, J.W. Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany. strebhardt@em.uni-frankfurt.de
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The polo-like kinase 1 (PLK1) acts in concert with cyclin-dependent kinase 1-cyclin B1 and Aurora kinases to orchestrate a wide range of critical cell cycle events. Because PLK1 has been preclinically validated as a cancer target, small-molecule inhibitors of PLK1 have become attractive candidates for anticancer drug development. Although the roles of the closely related PLK2, PLK3 and PLK4 in cancer are less well understood, there is evidence showing that PLK2 and PLK3 act as tumour suppressors through their functions in the p53 signalling network, which guards the cell against various stress signals. In this article, recent insights into the biology of PLKs will be reviewed, with an emphasis on their role in malignant transformation, and progress in the development of small-molecule PLK1 inhibitors will be examined.

Indexed as

AnimalsAntineoplastic AgentsCell Cycle ProteinsDrug Delivery SystemsDrug DesignHumansNeoplasmsPolo-Like Kinase 1Polo-like KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsTumor Suppressor Protein p53Tumor Suppressor ProteinsAntineoplastic AgentsCell Cycle ProteinsPLK2 protein, humanPLK3 protein, humanPLK4 protein, humanPolo-Like Kinase 1Polo-like KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20671765
OpenAlexW2037874673

What OpenQuestion holds

Textmetadata
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.