Fig 1.
Flowchart of MR investigating the causal relationship between LTL and PCa.
GIV assumptions: (1) GIVs must be strongly associated with LTL (P < 5×10−8); (2) GIVs must not be correlated with unmeasured confounders of the LTL and PCa relationship; (3) GIVs should only affect the risk of PCa through LTL. SNPs = single-nucleotide polymorphisms; LTL = leukocyte telomere length; PCa = prostate cancer; IVW = inverse-variance-weighted; WM = weighted median.
Table 1.
MR results of LTL on the risk of PCa.
Fig 2.
Scatter plots of LTL with the risk of PCa.
A–D, Effect of LTL-related SNPs on the PCa risk from four different cohorts. Scatter plot demonstrating the effect of each LTL-associated SNP on PCa on the log-odds scale. Slopes of each line represent the causal association for each method. MR = Mendelian randomization; SNP = single-nucleotide polymorphism; LTL = leukocyte telomere length; PCa = prostate cancer.
Fig 3.
Density plots of LTL with the risk of PCa.
A–D, Effect of LTL-related SNPs on the PCa risk from four different cohorts. MR = Mendelian randomization; SNP = single nucleotide polymorphism.
Fig 4.
Forest plots to visualize the results of the meta-analysis of the four different cohorts.
Forest plots demonstrating the average genetically determined effect of LTL on PCa. Presented OR and CI correspond to the average effects of LTL on PCa. I2 statistic and chi-squared-based Q were used to evaluate the heterogeneity among different studies.