Genome-wide association scan identifies a colorectal cancer susceptibility locus on 11q23 and replicates risk loci at 8q24 and 18q21.


Tenesa, A; Farrington, SM; Prendergast, JG; Porteous, ME; Walker, M; Haq, N; Barnetson, RA; Theodoratou, E; Cetnarskyj, R; Cartwright, N; Semple, C; Clark, AJ; Reid, FJ; Smith, LA; Kavoussanakis, K; Koessler, T; Pharoah, PD; Buch, S; Schafmayer, C; Tepel, J; Schreiber, S; Völzke, H; Schmidt, CO; Hampe, J; Chang-Claude, J; Hoffmeister, M; Brenner, H; Wilkening, S; Canzian, F; Capella, G; Moreno, V; Deary, IJ; Starr, JM; Tomlinson, IP; Kemp, Z; Howarth, K; Carvajal-Carmona, L; Webb, E; Broderick, P; Vijayakrishnan, J; Houlston, RS; Rennert, G; Ballinger, D; Rozek, L; Gruber, SB; Matsuda, K; Kidokoro, T; Nakamura, Y; Zanke, BW; Greenwood, CM; Rangrej, J; Kustra, R; Montpetit, A; Hudson, TJ; Gallinger, S; Campbell, H; Dunlop, MG; (2008) Genome-wide association scan identifies a colorectal cancer susceptibility locus on 11q23 and replicates risk loci at 8q24 and 18q21. Nature genetics, 40 (5). pp. 631-7. ISSN 1061-4036 DOI: https://doi.org/10.1038/ng.133

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Abstract

In a genome-wide association study to identify loci associated with colorectal cancer (CRC) risk, we genotyped 555,510 SNPs in 1,012 early-onset Scottish CRC cases and 1,012 controls (phase 1). In phase 2, we genotyped the 15,008 highest-ranked SNPs in 2,057 Scottish cases and 2,111 controls. We then genotyped the five highest-ranked SNPs from the joint phase 1 and 2 analysis in 14,500 cases and 13,294 controls from seven populations, and identified a previously unreported association, rs3802842 on 11q23 (OR = 1.1; P = 5.8 x 10(-10)), showing population differences in risk. We also replicated and fine-mapped associations at 8q24 (rs7014346; OR = 1.19; P = 8.6 x 10(-26)) and 18q21 (rs4939827; OR = 1.2; P = 7.8 x 10(-28)). Risk was greater for rectal than for colon cancer for rs3802842 (P < 0.008) and rs4939827 (P < 0.009). Carrying all six possible risk alleles yielded OR = 2.6 (95% CI = 1.75-3.89) for CRC. These findings extend our understanding of the role of common genetic variation in CRC etiology.

Item Type: Article
Faculty and Department: Faculty of Epidemiology and Population Health > Dept of Infectious Disease Epidemiology
PubMed ID: 18372901
Web of Science ID: 255366700032
URI: http://researchonline.lshtm.ac.uk/id/eprint/2439

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