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Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma

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Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma : Insights from genome-wide association studies. / Böhmer, Anne Christin; Hecker, Julian; Schröder, Julia; Gharahkhani, Puya; May, Andrea; Gerges, Christian; Anders, Mario; Becker, Jessica; Hess, Timo; Kreuser, Nicole; Thieme, Rene; Noder, Tania; Venerito, Marino; Veits, Lothar; Schmidt, Thomas; Fuchs, Claudia; Izbicki, Jakob R; Hölscher, Arnulf H; Dietrich, Arne; Moulla, Yusef; Lyros, Orestis; Lang, Hauke; Lorenz, Dietmar; Schumacher, Brigitte; Meyershofer, Rupert; Vashist, Yogesh K; Ott, Katja; Vieth, Michael; Weissmüller, Josef; Moebus, Susanne; Knapp, Michael; Neuhaus, Horst; Rösch, Thomas; Ell, Christian; Nöthen, Markus M; Whiteman, David C; Tomlinson, Ian; Jankowski, Janusz A; Fitzgerald, Rebecca C; Palles, Claire; Vaughan, Thomas L; Gockel, Ines; Thrift, Aaron P; Fier, Heide; Schumacher, Johannes.

In: CANCER EPIDEM BIOMAR, Vol. 29, No. 2, 02.2020, p. 427-433.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Böhmer, AC, Hecker, J, Schröder, J, Gharahkhani, P, May, A, Gerges, C, Anders, M, Becker, J, Hess, T, Kreuser, N, Thieme, R, Noder, T, Venerito, M, Veits, L, Schmidt, T, Fuchs, C, Izbicki, JR, Hölscher, AH, Dietrich, A, Moulla, Y, Lyros, O, Lang, H, Lorenz, D, Schumacher, B, Meyershofer, R, Vashist, YK, Ott, K, Vieth, M, Weissmüller, J, Moebus, S, Knapp, M, Neuhaus, H, Rösch, T, Ell, C, Nöthen, MM, Whiteman, DC, Tomlinson, I, Jankowski, JA, Fitzgerald, RC, Palles, C, Vaughan, TL, Gockel, I, Thrift, AP, Fier, H & Schumacher, J 2020, 'Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma: Insights from genome-wide association studies', CANCER EPIDEM BIOMAR, vol. 29, no. 2, pp. 427-433. https://doi.org/10.1158/1055-9965.EPI-19-0374

APA

Böhmer, A. C., Hecker, J., Schröder, J., Gharahkhani, P., May, A., Gerges, C., Anders, M., Becker, J., Hess, T., Kreuser, N., Thieme, R., Noder, T., Venerito, M., Veits, L., Schmidt, T., Fuchs, C., Izbicki, J. R., Hölscher, A. H., Dietrich, A., ... Schumacher, J. (2020). Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma: Insights from genome-wide association studies. CANCER EPIDEM BIOMAR, 29(2), 427-433. https://doi.org/10.1158/1055-9965.EPI-19-0374

Vancouver

Böhmer AC, Hecker J, Schröder J, Gharahkhani P, May A, Gerges C et al. Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma: Insights from genome-wide association studies. CANCER EPIDEM BIOMAR. 2020 Feb;29(2):427-433. https://doi.org/10.1158/1055-9965.EPI-19-0374

Bibtex

@article{ce3db8947fa14d8f81c7409c49081253,
title = "Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma: Insights from genome-wide association studies",
abstract = "BACKGROUND: Obesity is a major risk factor for esophageal adenocarcinoma (EA) and its precursor Barrett's esophagus (BE). Research suggests that individuals with high genetic risk to obesity have a higher BE/EA risk. To facilitate understanding of biological factors that lead to progression from BE to EA, the present study investigated the shared genetic background of BE/EA and obesity-related traits.METHODS: Cross-trait linkage disequilibrium score regression was applied to summary statistics from genome-wide association meta-analyses on BE/EA and on obesity traits. Body mass index (BMI) was used as a proxy for general obesity, and waist-to-hip ratio (WHR) for abdominal obesity. For single marker analyses, all genome-wide significant risk alleles for BMI and WHR were compared with summary statistics of the BE/EA meta-analyses.RESULTS: Sex-combined analyses revealed a significant genetic correlation between BMI and BE/EA (rg = 0.13, P = 2 × 10-04) and a rg of 0.12 between WHR and BE/EA (P = 1 × 10-02). Sex-specific analyses revealed a pronounced genetic correlation between BMI and EA in females (rg = 0.17, P = 1.2 × 10-03), and WHR and EA in males (rg = 0.18, P = 1.51 × 10-02). On the single marker level, significant enrichment of concordant effects was observed for BMI and BE/EA risk variants (P = 8.45 × 10-03) and WHR and BE/EA risk variants (P = 2 × 10-02).CONCLUSIONS: Our study provides evidence for sex-specific genetic correlations that might reflect specific biological mecha-nisms. The data demonstrate that shared genetic factors are particularly relevant in progression from BE to EA.IMPACT: Our study quantifies the genetic correlation between BE/EA and obesity. Further research is now warranted to elucidate these effects and to understand the shared pathophysiology.",
author = "B{\"o}hmer, {Anne Christin} and Julian Hecker and Julia Schr{\"o}der and Puya Gharahkhani and Andrea May and Christian Gerges and Mario Anders and Jessica Becker and Timo Hess and Nicole Kreuser and Rene Thieme and Tania Noder and Marino Venerito and Lothar Veits and Thomas Schmidt and Claudia Fuchs and Izbicki, {Jakob R} and H{\"o}lscher, {Arnulf H} and Arne Dietrich and Yusef Moulla and Orestis Lyros and Hauke Lang and Dietmar Lorenz and Brigitte Schumacher and Rupert Meyershofer and Vashist, {Yogesh K} and Katja Ott and Michael Vieth and Josef Weissm{\"u}ller and Susanne Moebus and Michael Knapp and Horst Neuhaus and Thomas R{\"o}sch and Christian Ell and N{\"o}then, {Markus M} and Whiteman, {David C} and Ian Tomlinson and Jankowski, {Janusz A} and Fitzgerald, {Rebecca C} and Claire Palles and Vaughan, {Thomas L} and Ines Gockel and Thrift, {Aaron P} and Heide Fier and Johannes Schumacher",
note = "{\textcopyright}2019 American Association for Cancer Research.",
year = "2020",
month = feb,
doi = "10.1158/1055-9965.EPI-19-0374",
language = "English",
volume = "29",
pages = "427--433",
journal = "CANCER EPIDEM BIOMAR",
issn = "1055-9965",
publisher = "American Association for Cancer Research Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Shared genetic etiology of obesity-related traits and Barrett's esophagus/adenocarcinoma

T2 - Insights from genome-wide association studies

AU - Böhmer, Anne Christin

AU - Hecker, Julian

AU - Schröder, Julia

AU - Gharahkhani, Puya

AU - May, Andrea

AU - Gerges, Christian

AU - Anders, Mario

AU - Becker, Jessica

AU - Hess, Timo

AU - Kreuser, Nicole

AU - Thieme, Rene

AU - Noder, Tania

AU - Venerito, Marino

AU - Veits, Lothar

AU - Schmidt, Thomas

AU - Fuchs, Claudia

AU - Izbicki, Jakob R

AU - Hölscher, Arnulf H

AU - Dietrich, Arne

AU - Moulla, Yusef

AU - Lyros, Orestis

AU - Lang, Hauke

AU - Lorenz, Dietmar

AU - Schumacher, Brigitte

AU - Meyershofer, Rupert

AU - Vashist, Yogesh K

AU - Ott, Katja

AU - Vieth, Michael

AU - Weissmüller, Josef

AU - Moebus, Susanne

AU - Knapp, Michael

AU - Neuhaus, Horst

AU - Rösch, Thomas

AU - Ell, Christian

AU - Nöthen, Markus M

AU - Whiteman, David C

AU - Tomlinson, Ian

AU - Jankowski, Janusz A

AU - Fitzgerald, Rebecca C

AU - Palles, Claire

AU - Vaughan, Thomas L

AU - Gockel, Ines

AU - Thrift, Aaron P

AU - Fier, Heide

AU - Schumacher, Johannes

N1 - ©2019 American Association for Cancer Research.

PY - 2020/2

Y1 - 2020/2

N2 - BACKGROUND: Obesity is a major risk factor for esophageal adenocarcinoma (EA) and its precursor Barrett's esophagus (BE). Research suggests that individuals with high genetic risk to obesity have a higher BE/EA risk. To facilitate understanding of biological factors that lead to progression from BE to EA, the present study investigated the shared genetic background of BE/EA and obesity-related traits.METHODS: Cross-trait linkage disequilibrium score regression was applied to summary statistics from genome-wide association meta-analyses on BE/EA and on obesity traits. Body mass index (BMI) was used as a proxy for general obesity, and waist-to-hip ratio (WHR) for abdominal obesity. For single marker analyses, all genome-wide significant risk alleles for BMI and WHR were compared with summary statistics of the BE/EA meta-analyses.RESULTS: Sex-combined analyses revealed a significant genetic correlation between BMI and BE/EA (rg = 0.13, P = 2 × 10-04) and a rg of 0.12 between WHR and BE/EA (P = 1 × 10-02). Sex-specific analyses revealed a pronounced genetic correlation between BMI and EA in females (rg = 0.17, P = 1.2 × 10-03), and WHR and EA in males (rg = 0.18, P = 1.51 × 10-02). On the single marker level, significant enrichment of concordant effects was observed for BMI and BE/EA risk variants (P = 8.45 × 10-03) and WHR and BE/EA risk variants (P = 2 × 10-02).CONCLUSIONS: Our study provides evidence for sex-specific genetic correlations that might reflect specific biological mecha-nisms. The data demonstrate that shared genetic factors are particularly relevant in progression from BE to EA.IMPACT: Our study quantifies the genetic correlation between BE/EA and obesity. Further research is now warranted to elucidate these effects and to understand the shared pathophysiology.

AB - BACKGROUND: Obesity is a major risk factor for esophageal adenocarcinoma (EA) and its precursor Barrett's esophagus (BE). Research suggests that individuals with high genetic risk to obesity have a higher BE/EA risk. To facilitate understanding of biological factors that lead to progression from BE to EA, the present study investigated the shared genetic background of BE/EA and obesity-related traits.METHODS: Cross-trait linkage disequilibrium score regression was applied to summary statistics from genome-wide association meta-analyses on BE/EA and on obesity traits. Body mass index (BMI) was used as a proxy for general obesity, and waist-to-hip ratio (WHR) for abdominal obesity. For single marker analyses, all genome-wide significant risk alleles for BMI and WHR were compared with summary statistics of the BE/EA meta-analyses.RESULTS: Sex-combined analyses revealed a significant genetic correlation between BMI and BE/EA (rg = 0.13, P = 2 × 10-04) and a rg of 0.12 between WHR and BE/EA (P = 1 × 10-02). Sex-specific analyses revealed a pronounced genetic correlation between BMI and EA in females (rg = 0.17, P = 1.2 × 10-03), and WHR and EA in males (rg = 0.18, P = 1.51 × 10-02). On the single marker level, significant enrichment of concordant effects was observed for BMI and BE/EA risk variants (P = 8.45 × 10-03) and WHR and BE/EA risk variants (P = 2 × 10-02).CONCLUSIONS: Our study provides evidence for sex-specific genetic correlations that might reflect specific biological mecha-nisms. The data demonstrate that shared genetic factors are particularly relevant in progression from BE to EA.IMPACT: Our study quantifies the genetic correlation between BE/EA and obesity. Further research is now warranted to elucidate these effects and to understand the shared pathophysiology.

U2 - 10.1158/1055-9965.EPI-19-0374

DO - 10.1158/1055-9965.EPI-19-0374

M3 - SCORING: Journal article

C2 - 31748258

VL - 29

SP - 427

EP - 433

JO - CANCER EPIDEM BIOMAR

JF - CANCER EPIDEM BIOMAR

SN - 1055-9965

IS - 2

ER -