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llo E, Rizor A, Son DS, Lee J, Aschner M, et al. LRRK2 kinase plays a critical role in manganese-induced inflammation and apoptosis in microglia. PLoS One. 2019;14:e0210248. 104. Qiu Q, Zhang GJ, Ma T, Qian WB, Wang JY, Ye ZQ, et al. The yak genome and adaptation to life at Bcl-2 Inhibitor web higher altitude. Nat Genet. 2012;44:946. 105. Guo XQ, Chen FZ, Gao F, Li L, Liu K, You LJ, et al. CNSA: a data repository for archiving omics information. Database (Oxford). 2020; 2020: baaa055. 106. Chen FZ, You LJ, Yang F, et al. CNGBdb: China National GeneBank DataBase. Hereditas. 2020;42:79909.Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Lung cancer (LC) is related with higher morbidity and mortality prices and, hence, remains a really serious threat to human health (Torre et al., 2015; Siegel et al., 2020). LC is typically found at sophisticated stages resulting from inconspicuous symptoms at the early stage of disease along with the lack of productive and handy screening strategies (Nasim et al., 2019). Hence, risk components and biomarkers in the carcinogenesis and progression of LC ought to be explored for application in screening and clinical practice. Even though smoking is really a main risk factor, some LC individuals have no history of smoking, indicating that other components, like second-hand smoke, indoor air pollution, and genetic elements, can market the onset and progression of LC (Rivera and Wakelee, 2016). Molecular epidemiological and experimental studies have shown that genetic variations play crucial roles in the occurrence of LC (Malhotra et al., 2016). A single nucleotide polymorphism (SNP), which can be defined as a nucleotide variation with a frequency of higher than 1 within a population,Frontiers in Molecular Biosciences | frontiersin.orgSeptember 2021 | Volume 8 | ArticleLi et al.SNPs and Lung Cancer Riskis probably the most widespread type of genetic variation in the human genome. A developing variety of studies on relationships in between SNP and LC risk have been published in current years. Systematic testimonials and meta-analyses with relatively higher levels of epidemiological proof have summarized the associations among a SNP (or certain SNP) and LC danger, due to the fact the results happen to be somewhat inconsistent (Lau et al., 1998). Nevertheless, the associations identified by systematic evaluations and meta-analyses may be not precise owing towards the influence of many things, which include publication bias (Ioannidis, 2005). Dong et al. evaluated the results of meta-analyses and pooled analyses in addition to the false good report probability (FPRP) to COX-2 Activator custom synthesis summarize the genetic susceptibility to cancer and located only 11 important associations between genetic variations and LC danger (Dong et al., 2008). Marshall et al. mainly applied the results of meta-analyses to overview genetic susceptibility to LC which was identified using a candidate gene approach (Marshall and Christiani, 2013). In 2017, Liu et al. utilized the Venice criteria and FPRP to evaluate the results of meta-analyses to further summarize genetic associations with all the danger of LC and identified only 15 SNP with robust proof (Liu et al., 2017). Nonetheless, to the greatest of our knowledge, an umbrella assessment that extracts data, as opposed to the outcomes, of systematic evaluations and meta-analyses to calculate and evaluate the associations among SNP and LC risk has not been reported at present. For that reason, in order to comprehensively and accurately assess the relationships involving SNP and

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