Evidence map›Paper›PMID 24265276›Full record

ReviewCancer research2013

The role of polo-like kinase 1 in carcinogenesis: cause or consequence?

Brian D Cholewa, Xiaoqi Liu, Nihal Ahmad

Open access · greenAbstract readReview
In one paragraph

Review in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  14. Targeting ST8SIA6-AS1 counteracts KRASExperimental hematology & oncology · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. The Anaphase-Promoting Complex/Cyclosome Is a Cellular Ageing Regulator.International journal of molecular sciences · 2022
    Review
  20. Article

29 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

3 authors at 2 institutions in 1 country.

Brian D CholewaAuthors' Affiliations: Department of Dermatology; Molecular and Environmental Toxicology Center, University of Wisconsin; William S. Middleton Memorial VA Hospital, Madison, Wisconsin; and Department of Biochemistry, Purdue University, West Lafayette, Indiana.
Xiaoqi Liu
Nihal Ahmad
William S. Middleton Memorial Veterans Hospital · USPurdue University West Lafayette · US

Funding

Molecular & Environmental Toxicology Pre-& Postdoctoral Training ProgramT32ES007015 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI CHRISTOPHER A BRADFIELD · 1985 to 2026
$11.5M
Role of Polo-Like Kinase-1 in Melanocytic TransformationR01AR059130 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI AHMAD, NIHAL · 2010 to 2019
$3.8M
Plk1 in Chemo-resistance of CancerR01CA157429 · NCI · UNIVERSITY OF KENTUCKY · PI XIAOQI LIU · 2011 to 2026
$3.5M
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 CA157429NCI NIH HHS R01CA157429NCI NIH HHS R01 CA176748NCI NIH HHS R01CA176748NIAMS NIH HHS R01 AR059130NIAMS NIH HHS R01AR059130NIEHS NIH HHS T32 ES007015NIEHS NIH HHS T32 ES007015-35
6 · The paper itself

Abstract

Polo-like kinase 1 (Plk1) is a well-established mitotic regulator with a diverse range of biologic functions continually being identified throughout the cell cycle. Preclinical evidence suggests that the molecular targeting of Plk1 could be an effective therapeutic strategy in a wide range of cancers; however, that success has yet to be translated to the clinical level. The lack of clinical success has raised the question of whether there is a true oncogenic addiction to Plk1 or if its overexpression in tumors is solely an artifact of increased cellular proliferation. In this review, we address the role of Plk1 in carcinogenesis by discussing the cell cycle and DNA damage response with respect to their associations with classic oncogenic and tumor suppressor pathways that contribute to the transcriptional regulation of Plk1. A thorough examination of the available literature suggests that Plk1 activity can be dysregulated through key transformative pathways, including both p53 and pRb. On the basis of the available literature, it may be somewhat premature to draw a definitive conclusion on the role of Plk1 in carcinogenesis. However, evidence supports the notion that oncogene dependence on Plk1 is not a late occurrence in carcinogenesis and it is likely that Plk1 plays an active role in carcinogenic transformation.

Indexed as

AnimalsCarcinogenesisCell CycleCell Cycle ProteinsCell ProliferationGenes, p53Genes, Tumor SuppressorHumansMitosisOncogenesPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsCell Cycle ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene Proteins

Identifiers

PMID24265276
PMCPMC3849226
OpenAlexW2134694638

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.