Evidence map›Paper›PMID 27330107›Full record

ReviewMolecular cancer therapeutics2016

Plk1 Inhibitors in Cancer Therapy: From Laboratory to Clinics.

Rosie Elizabeth Ann Gutteridge, Mary Ann Ndiaye, Xiaoqi Liu, Nihal Ahmad

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cancer therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed
17.4field-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

240 citing papers in PubMed, 408 citations in OpenAlex.

  1. CCNE1 and PLK1 Mediate Resistance to Palbociclib in HR+/HER2- Metastatic Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Targeting PLK1 Reduces MMP10 to Enhance Radiosensitivity in HPV- Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. High-throughput virtual screening, identification andJournal of enzyme inhibition and medicinal chemistry · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

180 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

4 authors at 2 institutions in 1 country.

Rosie Elizabeth Ann GutteridgeDepartment of Dermatology, University of Wisconsin, Madison, Wisconsin.
Mary Ann NdiayeDepartment of Dermatology, University of Wisconsin, Madison, Wisconsin.
Xiaoqi LiuDepartment of Biochemistry, Purdue University, West Lafayette, Indiana.
Nihal AhmadDepartment of Dermatology, University of Wisconsin, Madison, Wisconsin. William S. Middleton Memorial VA Hospital, Madison, Wisconsin. nahmad@wisc.edu.
University of Wisconsin–Madison · USPurdue University West Lafayette · US

Funding

Role of Polo-Like Kinase-1 in Melanocytic TransformationR01AR059130 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI AHMAD, NIHAL · 2010 to 2019
$3.8M
Role of SIRT1 in melanocyte biology and melanocyte transformationR01CA176748 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AHMAD, NIHAL · 2013 to 2017
$1.6M
Plk1-Numb Cooperation in MelanomagenesisI01BX001008 · VA · WM S. MIDDLETON MEMORIAL VETERANS HOSP · PI AHMAD, NIHAL · 2013 to 2016
–
BLRD VA I01 BX001008NCI NIH HHS R01 CA176748NIAMS NIH HHS R01 AR059130
6 · The paper itself

Abstract

Polo-like kinase 1 (Plk1) overexpression has been shown to occur in a wide range of tumors, prompting research and development of Plk1 inhibitors as a means of cancer treatment. This review discusses recent advances in the development of Plk1 inhibitors for cancer management. Plk1 inhibition has been shown to cause mitotic block and apoptosis of cells with higher mitotic index and therefore higher Plk1 expression. The potential of Plk1 inhibitors as cancer therapeutics has been widely investigated. However, a complete understanding of Plk1 biology/mechanism is yet to be fully achieved. Resistance to certain chemotherapeutic drugs has been linked to Plk1 overexpression, and Plk1-mediated mitotic events such as microtubule rearrangement have been found to reduce the efficacy of chemotherapeutic agents. The Plk1 inhibitor volasertib has shown considerable promise in clinical studies, having reached phase III trials. However, preclinical success with Plk1 inhibitors has not translated well into clinical success. In our view, combined therapies targeting other relevant pathways together with Plk1 may be vital to combat issues observed with monotherapy, especially resistance. In addition, research should also be directed toward understanding the mechanisms of Plk1 and designing additional next generations of specific, potent Plk1 inhibitors to target cancer. Mol Cancer Ther; 15(7); 1427-35. ©2016 AACR.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCell CycleCell Cycle ProteinsClinical Trials as TopicDrug Evaluation, PreclinicalDrug Resistance, NeoplasmHumansNeoplasmsPhosphorylationPolo-Like Kinase 1Protein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsAntineoplastic AgentsCell Cycle ProteinsPolo-Like Kinase 1Protein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins

Identifiers

PMID27330107
PMCPMC4936921
OpenAlexW2467902526

What OpenQuestion holds

Textmetadata
LicenceTDM
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.