Association between p73 G4C14‐to‐A4T14 polymorphism and lung cancer risk: A systematic review and meta‐analysis

Objective This study was conducted to evaluate the relationship between the p73 G4C14‐to‐A4T14 polymorphism (hereafter, G4C14‐to‐A4T14) and lung cancer risk. Methods The studies on the relationship between G4C14‐A4T14 and lung cancer risk published as of November 5, 2018, were comprehensively search...

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Veröffentlicht in:The clinical respiratory journal 2021-06, Vol.15 (6), p.637-647
Hauptverfasser: Du, Fenghua, Wang, Xiaojun, Qin, Dandan, Zhu, Rongjun, Kong, Weibo, Kong, Xiangzhou, Min, Xuhong
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Sprache:eng
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Zusammenfassung:Objective This study was conducted to evaluate the relationship between the p73 G4C14‐to‐A4T14 polymorphism (hereafter, G4C14‐to‐A4T14) and lung cancer risk. Methods The studies on the relationship between G4C14‐A4T14 and lung cancer risk published as of November 5, 2018, were comprehensively searched in PubMed, Embase, the Cochrane Library, the Chinese Wanfang database, China National Knowledge Infrastructure (CNKI), and China Biology Medicine (CBM). The last update was on May 24, 2019. Statistical analysis was performed using Stata 12.0. Results The association between G4C14‐A4T14 and lung cancer risk was analyzed in nine studies. The findings indicate no association between G4C14‐to‐A4T14 and lung cancer risk (allele model: OR = 0.90, 95% CI: 0.73–1.11, I2 = 86.0%, P = .330; dominant model: OR = 0.93, 95% CI: 0.74–1.17, I2 = 82.6%, P = .551; recessive model: OR = 0.75, 95% CI: 0.50–1.13, I2 = 75.2%, P = .165; homozygote model: OR = 0.74, 95% CI: 0.47–1.17, I2 = 79.6%, P = .199; heterozygote model: OR = 0.98, 95% CI: 0.80–1.21, I2 = 75.8%, P = .879). The heterogeneity between subgroups by cancer types and genotyping method was significantly reduced. After the deletion of suspected duplicates, no association was found between G4C14‐to‐A4T14 and lung cancer susceptibility. Conclusion Our meta‐analysis confirms that G4C14‐to‐A4T14 is not significantly related to lung cancer risk.
ISSN:1752-6981
1752-699X
DOI:10.1111/crj.13335