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Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma

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Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma. / 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, Jan-Hinnerk; Karch, Hans-Werner; Ahlbrand, Constantin J; Arras, Michael; Hofer, Sebastian; Mangold, Elisabeth; Heilmann-Heimbach, 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; Müller-Myhsok, 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.

in: CANCER RES, Jahrgang 4, Nr. 11, 11.2015, S. 1700-4.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Becker, J, May, A, Gerges, C, Anders, M, Veits, L, Weise, K, Czamara, D, Lyros, O, Manner, H, Terheggen, G, Venerito, M, Noder, T, Mayershofer, R, Hofer, J-H, Karch, H-W, Ahlbrand, CJ, Arras, M, Hofer, S, Mangold, E, Heilmann-Heimbach, S, Heinrichs, SKM, Hess, T, Kiesslich, R, Izbicki, JR, Hölscher, AH, Bollschweiler, E, Malfertheiner, P, Lang, H, Moehler, M, Lorenz, D, Müller-Myhsok, B, Ott, K, Schmidt, T, Whiteman, DC, Vaughan, TL, Nöthen, MM, Hackelsberger, A, Schumacher, B, Pech, O, Vashist, Y, Vieth, M, Weismüller, J, Neuhaus, H, Rösch, T, Ell, C, Gockel, I & Schumacher, J 2015, 'Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma', CANCER RES, Jg. 4, Nr. 11, S. 1700-4. https://doi.org/10.1002/cam4.500

APA

Becker, J., May, A., Gerges, C., Anders, M., Veits, L., Weise, K., Czamara, D., Lyros, O., Manner, H., Terheggen, G., Venerito, M., Noder, T., Mayershofer, R., Hofer, J-H., Karch, H-W., Ahlbrand, C. J., Arras, M., Hofer, S., Mangold, E., ... Schumacher, J. (2015). Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma. CANCER RES, 4(11), 1700-4. https://doi.org/10.1002/cam4.500

Vancouver

Becker J, May A, Gerges C, Anders M, Veits L, Weise K et al. Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma. CANCER RES. 2015 Nov;4(11):1700-4. https://doi.org/10.1002/cam4.500

Bibtex

@article{29720ef3c3d943f0a09e5084f7cc7583,
title = "Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma",
abstract = "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 CRTC1, FOXP1, and BARX1. Furthermore, they replicated an association at the FOXF1 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 SNPs in an independent sample consisting of 1065 EAC cases and 1019 controls of German descent. We could replicate the association at FOXP1, BARX1, and FOXF1 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 XRCC2 and GATA6 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.",
author = "Jessica Becker and Andrea May and Christian Gerges and Mario Anders and Lothar Veits and Katharina Weise and Darina Czamara and Orestis Lyros and Hendrik Manner and Grischa Terheggen and Marino Venerito and Tania Noder and Rupert Mayershofer and Jan-Hinnerk Hofer and Hans-Werner Karch and Ahlbrand, {Constantin J} and Michael Arras and Sebastian Hofer and Elisabeth Mangold and Stefanie Heilmann-Heimbach and Heinrichs, {Sophie K M} and Timo Hess and Ralf Kiesslich and Izbicki, {Jakob R} and H{\"o}lscher, {Arnulf H} and Elfriede Bollschweiler and Peter Malfertheiner and Hauke Lang and Markus Moehler and Dietmar Lorenz and Bertram M{\"u}ller-Myhsok and Katja Ott and Thomas Schmidt and Whiteman, {David C} and Vaughan, {Thomas L} and N{\"o}then, {Markus M} and Andreas Hackelsberger and Brigitte Schumacher and Oliver Pech and Yogesh Vashist and Michael Vieth and Josef Weism{\"u}ller and Horst Neuhaus and Thomas R{\"o}sch and Christian Ell and Ines Gockel and Johannes Schumacher",
note = "{\textcopyright} 2015 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.",
year = "2015",
month = nov,
doi = "10.1002/cam4.500",
language = "English",
volume = "4",
pages = "1700--4",
journal = "CANCER RES",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "11",

}

RIS

TY - JOUR

T1 - Supportive evidence for FOXP1, BARX1, and FOXF1 as genetic risk loci for the development of esophageal adenocarcinoma

AU - Becker, Jessica

AU - May, Andrea

AU - Gerges, Christian

AU - Anders, Mario

AU - Veits, Lothar

AU - Weise, Katharina

AU - Czamara, Darina

AU - Lyros, Orestis

AU - Manner, Hendrik

AU - Terheggen, Grischa

AU - Venerito, Marino

AU - Noder, Tania

AU - Mayershofer, Rupert

AU - Hofer, Jan-Hinnerk

AU - Karch, Hans-Werner

AU - Ahlbrand, Constantin J

AU - Arras, Michael

AU - Hofer, Sebastian

AU - Mangold, Elisabeth

AU - Heilmann-Heimbach, Stefanie

AU - Heinrichs, Sophie K M

AU - Hess, Timo

AU - Kiesslich, Ralf

AU - Izbicki, Jakob R

AU - Hölscher, Arnulf H

AU - Bollschweiler, Elfriede

AU - Malfertheiner, Peter

AU - Lang, Hauke

AU - Moehler, Markus

AU - Lorenz, Dietmar

AU - Müller-Myhsok, Bertram

AU - Ott, Katja

AU - Schmidt, Thomas

AU - Whiteman, David C

AU - Vaughan, Thomas L

AU - Nöthen, Markus M

AU - Hackelsberger, Andreas

AU - Schumacher, Brigitte

AU - Pech, Oliver

AU - Vashist, Yogesh

AU - Vieth, Michael

AU - Weismüller, Josef

AU - Neuhaus, Horst

AU - Rösch, Thomas

AU - Ell, Christian

AU - Gockel, Ines

AU - Schumacher, Johannes

N1 - © 2015 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

PY - 2015/11

Y1 - 2015/11

N2 - 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 CRTC1, FOXP1, and BARX1. Furthermore, they replicated an association at the FOXF1 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 SNPs in an independent sample consisting of 1065 EAC cases and 1019 controls of German descent. We could replicate the association at FOXP1, BARX1, and FOXF1 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 XRCC2 and GATA6 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.

AB - 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 CRTC1, FOXP1, and BARX1. Furthermore, they replicated an association at the FOXF1 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 SNPs in an independent sample consisting of 1065 EAC cases and 1019 controls of German descent. We could replicate the association at FOXP1, BARX1, and FOXF1 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 XRCC2 and GATA6 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.

U2 - 10.1002/cam4.500

DO - 10.1002/cam4.500

M3 - SCORING: Journal article

C2 - 26383589

VL - 4

SP - 1700

EP - 1704

JO - CANCER RES

JF - CANCER RES

SN - 0008-5472

IS - 11

ER -