Evidence map›Paper›PMID 31119048›Full record

ArticleCancer biology & medicine2019

p53 mutation regulates PKD genes and results in co-occurrence of PKD and tumorigenesis.

Haili Li, Yongjin Zhang, Juhua Dan, Ruoyu Zhou, Cui Li, Rong Li, Xiaoming Wu, Sanjay Kumar Singh, Jeffrey T Chang, Julun Yang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 10 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

11 authors at 5 institutions in 2 countries.

Haili LiFaculty of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming 650500, China.
Yongjin ZhangLaboratory of Molecular Genetics of Aging & Tumor, Kunming University of Science and Technology, Kunming 650500, China.
Juhua DanLaboratory of Molecular Genetics of Aging & Tumor, Kunming University of Science and Technology, Kunming 650500, China.
Ruoyu ZhouLaboratory of Molecular Genetics of Aging & Tumor, Kunming University of Science and Technology, Kunming 650500, China.
Cui LiLaboratory of Molecular Genetics of Aging & Tumor, Kunming University of Science and Technology, Kunming 650500, China.
Rong LiDivision of Nephrology, The First People's Hospital of Yunnan Province, Kunming 650032, China.
Xiaoming WuLaboratory of Molecular Genetics of Aging & Tumor, Kunming University of Science and Technology, Kunming 650500, China.
Sanjay Kumar SinghDepartment of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston 77030, TX, USA.
Jeffrey T ChangDepartment of Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, Houston 77030, TX, USA.
Julun YangDepartment of Pathology, Kunming General Hospital, Kunming 650032, China.
Ying LuoFaculty of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming 650500, China.
Kunming University of Science and Technology · CNFirst People's Hospital of Yunnan Province · CNThe First Hospital of Kunming · CNThe University of Texas Health Science Center at Houston · USThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePolycystic kidney disease (PKD) is the major cause of kidney failure and mortality in humans. It has always been suspected that the development of cystic kidney disease shares features with tumorigenesis, although the evidence is unclear.

methodsWe crossed p53 mutant mice (p53N236S, p53S) with Werner syndrome mice and analyzed the pathological phenotypes. The RNA-seq, ssGSEA analysis, and real-time PCR were performed to dissect the gene signatures involved in the development of disease phenotypes.

resultsWe found enlarged kidneys with fluid-filled cysts in offspring mice with a genotype of G3

conclusionsWe established a dual mouse model for PKD and tumorigenesis derived from abnormal cellular proliferation and telomere dysfunction. The innovative point of our study is to report PKD occurring in conjunction with tumorigenesis. The gene signatures revealed might shed new light on the pathogenesis of PKD, and provide new molecular biomarkers for clinical diagnosis and prognosis.

Indexed as

p53 mutationpolycystic kidney diseasetelomere dysfunctiontumorigenesis

Identifiers

PMID31119048
PMCPMC6528458
OpenAlexW2933382608

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.