Results: 2

1.
Figure 1

Figure 1. From: Association between genetic variants in the 8q24 cancer risk regions and circulating levels of androgens and sex-hormone binding globulin.

Figure 1 shows the summary graph of -log10 of P-values from linear regression analysis of the associations between all 164 SNPs typed within a 727 kb region of chromosome 8q24 and 4 serum androgen measures and SHBG plotted against the chromosomal locations of each SNP. Of the 164 SNPs analyzed, 24 were associated with serum androgens or SHBG at P<0.05, with 6 reaching P<0.01; a total of 30 tests were significant at P<0.05, with 10 reaching P<0.01. Similar results were found when analyzing androgens and SHBG in quartiles and quintiles or comparing highest to the lowest levels (data not shown). Additional adjustment for hour of blood draw to account for variations in circadian variation serum androgen levels (23, 24) did not change the results (data not shown).

Lisa W. Chu, et al. Cancer Epidemiol Biomarkers Prev. ;19(7):1848-1854.
2.
Figure 2

Figure 2. From: Association between genetic variants in the 8q24 cancer risk regions and circulating levels of androgens and sex-hormone binding globulin.

The strongest associations seen are for 3 adjacent SNPs at the centromeric end of prostate cancer risk region 2 (rs12334903, rs1456310, and rs980171) with total and bioavailable testosterone (P ≤ 1.13×10−3 and 6.28×10−4, respectively; Table 2 and Supplemental Table 1). These three SNPs are in relatively strong LD with each other (D′ >0.88, r2>0.69) have similar minor allele frequencies (MAFs; 39–43%), and similar effects on testosterone (each copy of the risk allele is associated with an 8–10% decrease in mean testosterone levels). All three SNPs remained significantly associated with testosterone after adjusting for multiple comparison of 38 SNPs tested within region 2 (P<0.03); after adjusting for all 164 SNPs tested, rs980171 remained associated with total and bioavailable testosterone (P=0.039 and 0.023, respectively) and rs12334903 with bioavailable testosterone (P=0.049). The Kruskal-Wallis non-parametric ANOVA also show that median total and bioavailable testosterone levels differed significantly among groups defined by the genotypes of the 3 SNPs (nominal P<1.48×10−3 and 7.5×10−4, respectively; Figure 2). Also of note is the association of a cluster of 9 SNPs (128,541,502–128,607,399 bp) in prostate cancer region 1 with androstenedione (nominal P<0.05; Supplemental Table 1), with five of the 9 SNPs (rs1447295, rs4242382, rs4242384, rs7017300, and rs11988857) in relatively strong LD (D′ >0.89, r2>0.71); these SNPs did not remain significant after adjusting for multiple testing of 22 SNPs in region 1 (P<0.34).

Lisa W. Chu, et al. Cancer Epidemiol Biomarkers Prev. ;19(7):1848-1854.

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