期刊
HUMAN MOLECULAR GENETICS
卷 23, 期 17, 页码 4729-4737出版社
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddu177
关键词
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资金
- Cancer Research UK [C1298/A8362, C348/A12076]
- European Union [258236]
- FP7 collaborative project SYSCOL
- COST Action [BM1206]
- National Cancer Research Network
- NHS via the Biological Research Centre of the National Institute for Health Research at the Royal Marsden Hospital NHS Trust
- ICR
- Sir John Fisher Foundation
- Scottish Government Health Department, Chief Scientist Office [CZD/16/6]
- UK Medical Research Council
- Oxford Comprehensive Biomedical Research Centre
- EU FP7 CHIBCHA grant
- Wellcome Trust Centre for Human Genetics, Oxford [090532/Z/09/Z]
- Swedish Cancer Society
- Swedish Scientific Research Council
- Stockholm Cancer Foundation
- National Cancer Institute, National Institutes of Health under RFA [CA-95-011]
- National Cancer Institute, National Institutes of Health [U01CA122839]
- Cancer Research UK [16459, 15116, 12076, 13154] Funding Source: researchfish
- Chief Scientist Office [CZD/16/6/4] Funding Source: researchfish
- Medical Research Council [MC_U127527198, G1001799, MR/K018647/1, MC_PC_U127527198] Funding Source: researchfish
- MRC [MC_U127527198, MC_PC_U127527198, MR/K018647/1, G1001799] Funding Source: UKRI
To identify common variants influencing colorectal cancer (CRC) risk, we performed a meta-analysis of five genome-wide association studies, comprising 5626 cases and 7817 controls of European descent. We conducted replication of top ranked single nucleotide polymorphisms (SNPs) in additional series totalling 14 037 cases and 15 937 controls, identifying a new CRC risk locus at 10q24.2 [rs1035209; odds ratio (OR) = 1.13, P = 4.54 x 10(-11)]. We also performed meta-analysis of our studies, with previously published data, of several recently purported CRC risk loci. We failed to find convincing evidence for a previously reported genome-wide association at rs11903757 (2q32.3). Of the three additional loci for which evidence of an association in Europeans has been previously described we failed to show an association between rs59336 (12q24.21) and CRC risk. However, for the other two SNPs, our analyses demonstrated new, formally significant associations with CRC. These are rs3217810 intronic in CCND2 (12p13.32; OR = 1.19, P = 2.16 x 10(-10)) and rs10911251 near LAMC1 (1q25.3; OR = 1.09, P = 1.75 x 10(-8)). Additionally, we found some evidence to support a relationship between, rs647161, rs2423297 and rs10774214 and CRC risk originally identified in East Asians in our European datasets. Our findings provide further insights into the genetic and biological basis of inherited genetic susceptibility to CRC.
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