TitleTP53 common variants and interaction with PPP1R13L and CD3EAP SNPs and lung cancer risk and smoking behavior in a Chinese population
AuthorsYin, Jiaoyang
Hou, Wei
Vogel, Ulla
Li, Xinxin
Ma, Yegang
Wang, Chunhong
Wang, Huiwen
Sun, Zhenxiang
AffiliationShenyang Med Coll, Liaoning Educ Minist, Key Lab Environm & Populat Hlth, 146 Huanghe North St, Shenyang 110034, Liaoning, Peoples R China
Peking Univ, Dept Pathol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing,Canc Hosp & Inst, Beijing, Peoples R China
Natl Res Ctr Working Environm, DK-2100 Copenhagen, Denmark
Liaoning Canc Hosp, Dept Thorac Surg, Shenyang, Liaoning, Peoples R China
KeywordsSQUAMOUS-CELL CARCINOMA
CODON 72 POLYMORPHISM
CHROMOSOME 19Q13.3
ASSOCIATION
GENE
SUSCEPTIBILITY
PROMOTER
ARG72PRO
SMOKERS
REGION
Issue DateFeb-2022
PublisherBIOMEDICAL JOURNAL
AbstractBackground: TP53 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. Methods: We 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. Results: No 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 (rs12951053A-rs1042522C-rs8079544Crs12602273G-rs8064946C) [OR (95% CI) = 0.13 (0.03e0.59), p = 0.0079] was associated with decreased risk of lung cancer after adjusted for smoking-duration. The analysis of smoking-duration within TP53 haplotypes showed that there were more carriers of haplotype1 (AGCCG), 2 (CCCGC) and 4 (CCCCG) in smoking-subgroup of >20 (years) (all p < 0.05). MDR testing analysis identified two significant models (both p < 0.0010) of genegene-environment interaction in relation to lung cancer risk in whole study group. Conclusion: The 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.
URIhttp://hdl.handle.net/20.500.11897/649918
ISSN2319-4170
DOI10.1016/j.bj.2021.01.006
IndexedSCI(E)
Appears in Collections:北京肿瘤医院

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