PDF(Pubmed)
Abstract：
OBJECTIVE: Research has previously established connections between the intestinal microbiome and the progression of some cancers. However, there is a noticeable gap in the literature in regard to using Mendelian randomisation (MR) to delve into potential causal relationships between the gut microbiota (GM) and basal cell carcinoma (BCC). Therefore, the purpose of our study was to use MR to explore the causal relationship between four kinds of GM (Bacteroides, Streptococcus, Proteobacteria and Lachnospiraceae) and BCC.
METHODS: We used genome-wide association study (GWAS) data and MR to explore the causal relationship between four kinds of GM and BCC. This study primarily employed the random effect inverse variance weighted (IVW) model for analysis, as complemented by additional methods including the simple mode, weighted median, weighted mode and MR‒Egger methods. We used heterogeneity and horizontal multiplicity to judge the reliability of each analysis. MR-PRESSO was mainly used to detect and correct outliers.
RESULTS: The random-effects IVW results showed that Bacteroides (OR = 0.936, 95% CI = 0.787-1.113, p = 0.455), Streptococcus (OR = 0.974, 95% CI = 0.875-1.083, p = 0.629), Proteobacteria (OR = 1.113, 95% CI = 0.977-1.267, p = 0.106) and Lachnospiraceae (OR = 1.027, 95% CI = 0.899-1.173, p = 0.688) had no genetic causal relationship with BCC. All analyses revealed no horizontal pleiotropy, heterogeneity or outliers.
CONCLUSIONS: We found that Bacteroides, Streptococcus, Proteobacteria and Lachnospiraceae do not increase the incidence of BCC at the genetic level, which provides new insight for the study of GM and BCC.
METHODS: We used genome-wide association study (GWAS) data and MR to explore the causal relationship between four kinds of GM and BCC. This study primarily employed the random effect inverse variance weighted (IVW) model for analysis, as complemented by additional methods including the simple mode, weighted median, weighted mode and MR‒Egger methods. We used heterogeneity and horizontal multiplicity to judge the reliability of each analysis. MR-PRESSO was mainly used to detect and correct outliers.
RESULTS: The random-effects IVW results showed that Bacteroides (OR = 0.936, 95% CI = 0.787-1.113, p = 0.455), Streptococcus (OR = 0.974, 95% CI = 0.875-1.083, p = 0.629), Proteobacteria (OR = 1.113, 95% CI = 0.977-1.267, p = 0.106) and Lachnospiraceae (OR = 1.027, 95% CI = 0.899-1.173, p = 0.688) had no genetic causal relationship with BCC. All analyses revealed no horizontal pleiotropy, heterogeneity or outliers.
CONCLUSIONS: We found that Bacteroides, Streptococcus, Proteobacteria and Lachnospiraceae do not increase the incidence of BCC at the genetic level, which provides new insight for the study of GM and BCC.
摘要：
目的：研究先前已经建立了肠道微生物组和某些癌症进展之间的联系。然而,在使用孟德尔随机化(MR)研究肠道微生物群(GM)与基底细胞癌(BCC)之间的潜在因果关系方面,文献存在明显的差距.因此,我们研究的目的是利用MR来探索四种GM(拟杆菌，链球菌,变形杆菌和落叶草科）和BCC。
方法：我们使用全基因组关联研究（GWAS）数据和MR来探索四种GM与BCC之间的因果关系。本研究主要采用随机效应逆方差加权(IVW)模型进行分析，作为补充的额外的方法，包括简单的模式，加权中位数，加权模式和MR-Egger方法。我们使用异质性和水平多重性来判断每个分析的可靠性。MR-PRESSO主要用于检测和校正异常值。
结果：随机效应IVW结果显示拟杆菌（OR=0.936，95％CI=0.787-1.113，p=0.455），链球菌(OR=0.974,95%CI=0.875-1.083,p=0.629),变形杆菌(OR=1.113,95%CI=0.977-1.267,p=0.106)和落叶松科(OR=1.027,95%CI=0.899-1.173,p=0.688)与BCC无遗传因果关系。所有分析都显示没有水平多效性，异质性或异常值。
结论：我们发现拟杆菌，链球菌,变形杆菌和落叶草在基因水平上不会增加BCC的发病率，这为GM和BCC的研究提供了新的思路。
方法：我们使用全基因组关联研究（GWAS）数据和MR来探索四种GM与BCC之间的因果关系。本研究主要采用随机效应逆方差加权(IVW)模型进行分析，作为补充的额外的方法，包括简单的模式，加权中位数，加权模式和MR-Egger方法。我们使用异质性和水平多重性来判断每个分析的可靠性。MR-PRESSO主要用于检测和校正异常值。
结果：随机效应IVW结果显示拟杆菌（OR=0.936，95％CI=0.787-1.113，p=0.455），链球菌(OR=0.974,95%CI=0.875-1.083,p=0.629),变形杆菌(OR=1.113,95%CI=0.977-1.267,p=0.106)和落叶松科(OR=1.027,95%CI=0.899-1.173,p=0.688)与BCC无遗传因果关系。所有分析都显示没有水平多效性，异质性或异常值。
结论：我们发现拟杆菌，链球菌,变形杆菌和落叶草在基因水平上不会增加BCC的发病率，这为GM和BCC的研究提供了新的思路。
