Evidence map›Paper›PMID 35351459›Full record

ArticleBiomedical journal2022

TP53 common variants and interaction with PPP1R13L and CD3EAP SNPs and lung cancer risk and smoking behavior in a Chinese population.

Jiaoyang Yin, Wei Hou, Ulla Vogel, Xinxin Li, Yegang Ma, Chunhong Wang, Huiwen Wang, Zhenxiang Sun

Open access · goldAbstract read
In one paragraph

Article in Biomedical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. About gladiators and a sacred disease.Biomedical journal · 2022
    Article
  4. Article
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

8 authors at 4 institutions in 2 countries.

Jiaoyang YinKey Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang, Liaoning Province, People's Republic of China. Electronic address: yinjye@163.com.
Wei HouKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Pathology, Peking University Cancer Hospital & Institute, Beijing, People's Republic of China.
Ulla VogelNational Research Centre for the Working Environment, DK-2100 Copenhagen, Denmark.
Xinxin LiKey Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang, Liaoning Province, People's Republic of China.
Yegang MaDepartment of Thoracic Surgery, Liaoning Cancer Hospital, Shenyang, Liaoning Province, People's Republic of China.
Chunhong WangKey Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang, Liaoning Province, People's Republic of China.
Huiwen WangKey Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang, Liaoning Province, People's Republic of China.
Zhenxiang SunKey Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang, Liaoning Province, People's Republic of China.
Shenyang Medical College · CNLiaoning Cancer Hospital & Institute · CNNational Research Centre for the Working Environment · DKPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTP53 encodes a tumor suppressor protein containing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. The effect of TP53 inactivation is well-known, and genetically determined smaller variations in TP53 activity are related to cancer. Lung cancer causes the highest rates of morbidity and mortality in the world. Epidemiology studies have assessed the association of TP53 single nucleotide polymorphisms with lung cancer.

methodsWe systematically examined the association of five htSNPs (haplotype-tagging single nucleotide polymorphism) (rs12951053, rs1042522, rs8079544, rs12602273 and rs8064946) across the entire TP53 locus and interaction between genes TP53 and PPP1R13L and CD3EAP and smoking-duration related to lung cancer risk in this Chinese study including 544 cases and 550 controls.

resultsNo significant associations were observed in analysis of alleles and genotypes with co-dominant, dominant, recessive, and log-additive models after adjustment for smoking status. Haplotype analysis showed that haplotype9 (rs12951053

conclusionThe present results provide novel evidence that the haplotype of TP53 htSNPs and interaction between genetic variation in TP53 and CD3EAP and smoking-duration may associate with lung cancer risk, and provide additional evidence of association between TP53 htSNP haplotypes and long-term smoking-related behavior.

Indexed as

Intracellular Signaling Peptides and ProteinsLung NeoplasmsPolymorphism, Single NucleotideRepressor ProteinsRNA Polymerase ITumor Suppressor Protein p53Case-Control StudiesChinaGenetic Predisposition to DiseaseGenotypeHaplotypesHumansSmokingIntracellular Signaling Peptides and ProteinsPOLR1G protein, humanPPP1R13L protein, humanRepressor ProteinsRNA Polymerase ITP53 protein, humanTumor Suppressor Protein p53ChineseGenetic variantsInteractionLung cancerSmoking durationTP53 and PPP1R13L and CD3EAP

Identifiers

PMID35351459
PMCPMC9133261
OpenAlexW3128119254

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.