Evidence map›Paper›PMID 36194647›Full record

ArticleScience signaling2022

The kinase PLK1 promotes the development of

Yifan Kong, Derek B Allison, Qiongsi Zhang, Daheng He, Yuntong Li, Fengyi Mao, Chaohao Li, Zhiguo Li, Yanquan Zhang, Jianlin Wang and 3 more

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Yifan KongDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.ORCID 0000-0002-5650-8079
Derek B AllisonMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.ORCID 0000-0002-5119-2474
Qiongsi ZhangDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Daheng HeMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
Yuntong LiMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
Fengyi MaoDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Chaohao LiDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Zhiguo LiDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Yanquan ZhangDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.ORCID 0000-0003-3527-9972
Jianlin WangDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Chi WangMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.ORCID 0000-0001-8984-4995
Christine F BrainsonDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.ORCID 0000-0002-0854-5043
Xiaoqi LiuDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
Plk1 in Chemo-resistance of CancerR01CA157429 · NCI · UNIVERSITY OF KENTUCKY · PI XIAOQI LIU · 2011 to 2026
$3.5M
Improving chemotherapy of castration-resistant prostate cancer.R01CA196634 · NCI · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI · 2016 to 2025
$3.3M
Plk1 as a prognostic biomarker for prostate cancerR01CA264652 · NCI · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI · 2021 to 2025
$2.7M
Enhancing the efficacy of androgen signaling inhibitors in prostate cancerR01CA256893 · NCI · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI · 2021 to 2025
$2.4M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA157429NCI NIH HHS R01 CA196634NCI NIH HHS R01 CA256893NCI NIH HHS R01 CA264652
6 · The paper itself

Abstract

Increased abundance of polo-like kinase 1 (PLK1) is observed in various tumor types, particularly in lung adenocarcinoma (LUAD). Here, we found that PLK1 accelerated the progression of LUAD through a mechanism that was independent of its role in mediating mitotic cell division. Analysis of human tumor databases revealed that increased PLK1 abundance in LUAD correlated with mutations in KRAS and p53, with tumor stage, and with reduced survival in patients. In a mouse model of KRAS

Indexed as

Adenocarcinoma of LungLung NeoplasmsAnimalsCell Cycle ProteinsCell Line, TumorHumansMiceMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-retProto-Oncogene Proteins p21(ras)Transcriptional ActivationTranscription FactorsCell Cycle ProteinsHras protein, mouseKRAS protein, humanMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-retProto-Oncogene Proteins p21(ras)Ret protein, mouseTP53 protein, humanTranscription FactorsTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID36194647
PMCPMC9737055
OpenAlexW4301183272

What OpenQuestion holds

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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.