| Literature DB >> 28195142 |
Julius Gudmundsson1, Gudmar Thorleifsson1, Jon K Sigurdsson1, Lilja Stefansdottir1, Jon G Jonasson2,3,4, Sigurjon A Gudjonsson1, Daniel F Gudbjartsson1, Gisli Masson1, Hrefna Johannsdottir1, Gisli H Halldorsson1, Simon N Stacey1, Hannes Helgason1,5, Patrick Sulem1, Leigha Senter6, Huiling He7, Sandya Liyanarachchi7, Matthew D Ringel8, Esperanza Aguillo9, Angeles Panadero10, Enrique Prats11, Almudena Garcia-Castaño12, Ana De Juan12, Fernando Rivera12, Li Xu13, Lambertus A Kiemeney14, Gudmundur I Eyjolfsson15, Olof Sigurdardottir16, Isleifur Olafsson2, Hoskuldur Kristvinsson2, Romana T Netea-Maier17, Thorvaldur Jonsson2,3, Jose I Mayordomo18, Theo S Plantinga19, Hannes Hjartarson2, Jon Hrafnkelsson2, Erich M Sturgis13, Unnur Thorsteinsdottir1,3, Thorunn Rafnar1, Albert de la Chapelle7, Kari Stefansson1,3.
Abstract
The great majority of thyroid cancers are of the non-medullary type. Here we report findings from a genome-wide association study of non-medullary thyroid cancer, including in total 3,001 patients and 287,550 controls from five study groups of European descent. Our results yield five novel loci (all with Pcombined<3 × 10-8): 1q42.2 (rs12129938 in PCNXL2), 3q26.2 (rs6793295 a missense mutation in LRCC34 near TERC), 5q22.1 (rs73227498 between NREP and EPB41L4A), 10q24.33 (rs7902587 near OBFC1), and two independently associated variants at 15q22.33 (rs2289261 and rs56062135; both in SMAD3). We also confirm recently published association results from a Chinese study of a variant on 5p15.33 (rs2736100 near the TERT gene) and present a stronger association result for a moderately correlated variant (rs10069690; OR=1.20, P=3.2 × 10-7) based on our study of individuals of European ancestry. In combination, these results raise several opportunities for future studies of the pathogenesis of thyroid cancer.Entities:
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Year: 2017 PMID： 28195142 PMCID： PMC5316879 DOI： 10.1038/ncomms14517
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919