Open AccessSupportive evidence for FOXP 1 , BARX 1 , and FOXF 1 as genetic risk loci for the development of esophageal adenocarcinoma
Author(s) -
Becker Jessica,
May Andrea,
Gerges Christian,
Anders Mario,
Veits Lothar,
Weise Katharina,
Czamara Darina,
Lyros Orestis,
Manner Hendrik,
Terheggen Grischa,
Venerito Marino,
Noder Tania,
Mayershofer Rupert,
Hofer JanHinnerk,
Karch HansWerner,
Ahlbrand Constantin J.,
Arras Michael,
Hofer Sebastian,
Mangold Elisabeth,
HeilmannHeimbach Stefanie,
Heinrichs Sophie K. M.,
Hess Timo,
Kiesslich Ralf,
Izbicki Jakob R.,
Hölscher Arnulf H.,
Bollschweiler Elfriede,
Malfertheiner Peter,
Lang Hauke,
Moehler Markus,
Lorenz Dietmar,
MüllerMyhsok Bertram,
Ott Katja,
Schmidt Thomas,
Whiteman David C.,
Vaughan Thomas L.,
Nöthen Markus M.,
Hackelsberger Andreas,
Schumacher Brigitte,
Pech Oliver,
Vashist Yogesh,
Vieth Michael,
Weismüller Josef,
Neuhaus Horst,
Rösch Thomas,
Ell Christian,
Gockel Ines,
Schumacher Johannes
Publication year - 2015
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.500
Subject(s) - genome wide association study , single nucleotide polymorphism , genetic association , biology , genetics , esophageal adenocarcinoma , gene , snp , adenocarcinoma , genotype , cancer
The Barrett's and Esophageal Adenocarcinoma Consortium ( BEACON ) recently performed a genome‐wide association study ( GWAS ) on esophageal adenocarcinoma ( EAC ) and Barrett's esophagus. They identified genome‐wide significant association for variants at three genes, namely CRTC 1 , FOXP 1 , and BARX 1 . Furthermore, they replicated an association at the FOXF 1 gene that has been previously found in a GWAS on Barrett's esophagus. We aimed at further replicating the association at these and other loci that showed suggestive association with P < 10 −4 in the BEACON sample. In total, we tested 88 SNP s in an independent sample consisting of 1065 EAC cases and 1019 controls of German descent. We could replicate the association at FOXP 1 , BARX 1 , and FOXF 1 with nominal significance and thereby confirm that genetic variants at these genes confer EAC risk. In addition, we found association of variants near the genes XRCC 2 and GATA 6 that were strongly ( P < 10 −5 ) although not genome‐wide significantly associated with the BEACON GWAS . Therefore, both variants and corresponding genes represent promising candidates for future EAC association studies on independent samples.