Table 2 Summary statistics and fine-mapping for the CCVs in UK Biobank meta-analysis

From: Allelic effects on KLHL17 expression underlie a pancreatic cancer genome-wide association signal at chr1p36.33

aSNP, balleles, clocation

OR (95% CI)

P-value

LD r2

LLR

SuSiE PIP

Chromatin accessibility

rs13303010 (G, A) 1:894,573

1.24 (1.16-1.32)

2.09 × 10−10

--

1.00

0.27

Yes

rs3935066 (G, A) 1:900,730

1.25 (1.17-1.35)

2.74 × 10−10

0.89

1.30

0.22

No (>500 bp)

rs113491766 (A, AG) 1:895,755

0.81 (0.76-0.86)

2.85 × 10−10

1

1.35

0.20

~56 bp away

rs13303327 (G, A) 1:895,706

1.24 (1.16-1.32)

3.38 × 10−10

1

1.60

0.18

~110 bp away

rs10465241 (C, T) 1:886,817

1.24 (1.16-1.32)

1.03 × 10−9

0.90

4.74

0.06

~22 bp

rs10465242 (G, A) 1:886,788

1.23 (1.1.5-1.32)

2.23 × 10−9

0.90

10.07

0.03

~52 bp

rs13303160 (G, A) 1:901,559

1.23 (1.15-1.32)

2.74 × 10−9

0.93

12.31

0.02

Yes

  1. Summary statistics of the CCVs for the newest meta-analysis with PDAC UK Biobank cases and controls including OR and 95% CI, P-value, linkage disequilibrium (LD) r2 reported relative to the tag SNP based on the European 1000Genomes reference, likelihood ratio (LLR), SuSiE posterior inclusion probability (PIP), and proximity to accessible chromatin. GWAS statistics are generated using a logistic regression model adjusted for covariates outlined in the Methods. P-values are not multiple-testing corrected. LLR was calculated using the GWAS P-values and a chi-squared test. Top five SNPs were identified in the SuSiE credible set of variants. All variants listed met the fine-mapping criteria for functional follow-up. Accessible chromatin is based on the ATAC-seq data generated in PDAC-derived or normal-derived pancreas epithelial cell lines24. Source data are provided as a Source Data file.
  2. arsID.
  3. bMinor, major alleles.
  4. cchr:position (Genome build hg19).
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