Genetically Determined Height and Risk of Non-hodgkin Lymphoma

Amy Moore; Eleanor Kane; Zhaoming Wang; Orestis A. Panagiotou; Lauren R. Teras; Alain Monnereau; Nicole Wong Doo; Mitchell J. Machiela; Christine F. Skibola; Susan L. Slager; Gilles Salles; Nicola J. Camp; Paige M. Bracci; Alexandra Nieters; Roel C.H. Vermeulen; Joseph Vijai; Karin E. Smedby; Yawei Zhang; Claire M. Vajdic; Wendy Cozen; John J. Spinelli; Henrik Hjalgrim; Graham G. Giles; Brian K. Link; Jacqueline Clavel; Alan A. Arslan; Mark P. Purdue; Lesley F. Tinker; Demetrius Albanes; Giovanni M. Ferri; Thomas M. Habermann; Hans Olov Adami; Nikolaus Becker; Yolanda Benavente; Simonetta Bisanzi; Paolo Boffetta; Paul Brennan; Angela R. Brooks-Wilson; Federico Canzian; Lucia Conde; David G. Cox; Karen Curtin; Lenka Foretova; Susan M. Gapstur; Hervé Ghesquières; Martha Glenn; Bengt Glimelius; Rebecca D. Jackson; Qing Lan; Mark Liebow; Marc Maynadie; James McKay; Mads Melbye; Lucia Miligi; Roger L. Milne; Thierry J. Molina; Lindsay M. Morton; Kari E. North; Kenneth Offit; Marina Padoan; Alpa V. Patel; Sara Piro; Vignesh Ravichandran; Elio Riboli; Silvia de Sanjose; Richard K. Severson; Melissa C. Southey; Anthony Staines; Carolyn Stewart; Ruth C. Travis; Elisabete Weiderpass; Stephanie Weinstein; Tongzhang Zheng; Stephen J. Chanock; Nilanjan Chatterjee; Nathaniel Rothman; Brenda M. Birmann; James R. Cerhan; Sonja I. Berndt

doi:10.3389/fonc.2019.01539

Genetically Determined Height and Risk of Non-hodgkin Lymphoma

Amy Moore, Eleanor Kane, Zhaoming Wang, Orestis A. Panagiotou, Lauren R. Teras, Alain Monnereau, Nicole Wong Doo, Mitchell J. Machiela, Christine F. Skibola, Susan L. Slager, Gilles Salles, Nicola J. Camp, Paige M. Bracci, Alexandra Nieters, Roel C.H. Vermeulen, Joseph Vijai, Karin E. Smedby, Yawei Zhang, Claire M. Vajdic, Wendy CozenJohn J. Spinelli, Henrik Hjalgrim, Graham G. Giles, Brian K. Link, Jacqueline Clavel, Alan A. Arslan, Mark P. Purdue, Lesley F. Tinker, Demetrius Albanes, Giovanni M. Ferri, Thomas M. Habermann, Hans Olov Adami, Nikolaus Becker, Yolanda Benavente, Simonetta Bisanzi, Paolo Boffetta, Paul Brennan, Angela R. Brooks-Wilson, Federico Canzian, Lucia Conde, David G. Cox, Karen Curtin, Lenka Foretova, Susan M. Gapstur, Hervé Ghesquières, Martha Glenn, Bengt Glimelius, Rebecca D. Jackson, Qing Lan, Mark Liebow, Marc Maynadie, James McKay, Mads Melbye, Lucia Miligi, Roger L. Milne, Thierry J. Molina, Lindsay M. Morton, Kari E. North, Kenneth Offit, Marina Padoan, Alpa V. Patel, Sara Piro, Vignesh Ravichandran, Elio Riboli, Silvia de Sanjose, Richard K. Severson, Melissa C. Southey, Anthony Staines, Carolyn Stewart, Ruth C. Travis, Elisabete Weiderpass, Stephanie Weinstein, Tongzhang Zheng, Stephen J. Chanock, Nilanjan Chatterjee, Nathaniel Rothman, Brenda M. Birmann, James R. Cerhan, Sonja I. Berndt

Bloomberg School of Public Health

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00–1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01–1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.

Original language	English (US)
Article number	1539
Journal	Frontiers in Oncology
Volume	9
DOIs	https://doi.org/10.3389/fonc.2019.01539
State	Published - Jan 28 2020

Keywords

chronic lymphocytic leukemia
diffuse large B-cell lymphoma
follicular lymphoma
genetics
height
marginal zone lymphoma
non-Hodgkin lymphoma
polygenic risk score

ASJC Scopus subject areas

Oncology
Cancer Research

Access to Document

10.3389/fonc.2019.01539

Cite this

Moore, A., Kane, E., Wang, Z., Panagiotou, O. A., Teras, L. R., Monnereau, A., Wong Doo, N., Machiela, M. J., Skibola, C. F., Slager, S. L., Salles, G., Camp, N. J., Bracci, P. M., Nieters, A., Vermeulen, R. C. H., Vijai, J., Smedby, K. E., Zhang, Y., Vajdic, C. M., ... Berndt, S. I. (2020). Genetically Determined Height and Risk of Non-hodgkin Lymphoma. Frontiers in Oncology, 9, Article 1539. https://doi.org/10.3389/fonc.2019.01539

Moore, A, Kane, E, Wang, Z, Panagiotou, OA, Teras, LR, Monnereau, A, Wong Doo, N, Machiela, MJ, Skibola, CF, Slager, SL, Salles, G, Camp, NJ, Bracci, PM, Nieters, A, Vermeulen, RCH, Vijai, J, Smedby, KE, Zhang, Y, Vajdic, CM, Cozen, W, Spinelli, JJ, Hjalgrim, H, Giles, GG, Link, BK, Clavel, J, Arslan, AA, Purdue, MP, Tinker, LF, Albanes, D, Ferri, GM, Habermann, TM, Adami, HO, Becker, N, Benavente, Y, Bisanzi, S, Boffetta, P, Brennan, P, Brooks-Wilson, AR, Canzian, F, Conde, L, Cox, DG, Curtin, K, Foretova, L, Gapstur, SM, Ghesquières, H, Glenn, M, Glimelius, B, Jackson, RD, Lan, Q, Liebow, M, Maynadie, M, McKay, J, Melbye, M, Miligi, L, Milne, RL, Molina, TJ, Morton, LM, North, KE, Offit, K, Padoan, M, Patel, AV, Piro, S, Ravichandran, V, Riboli, E, de Sanjose, S, Severson, RK, Southey, MC, Staines, A, Stewart, C, Travis, RC, Weiderpass, E, Weinstein, S, Zheng, T, Chanock, SJ, Chatterjee, N, Rothman, N, Birmann, BM, Cerhan, JR & Berndt, SI 2020, 'Genetically Determined Height and Risk of Non-hodgkin Lymphoma', Frontiers in Oncology, vol. 9, 1539. https://doi.org/10.3389/fonc.2019.01539

@article{22a45b564f964d62b42f1010bc93c040,

title = "Genetically Determined Height and Risk of Non-hodgkin Lymphoma",

abstract = "Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00–1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01–1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.",

keywords = "chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, genetics, height, marginal zone lymphoma, non-Hodgkin lymphoma, polygenic risk score",

author = "Amy Moore and Eleanor Kane and Zhaoming Wang and Panagiotou, {Orestis A.} and Teras, {Lauren R.} and Alain Monnereau and {Wong Doo}, Nicole and Machiela, {Mitchell J.} and Skibola, {Christine F.} and Slager, {Susan L.} and Gilles Salles and Camp, {Nicola J.} and Bracci, {Paige M.} and Alexandra Nieters and Vermeulen, {Roel C.H.} and Joseph Vijai and Smedby, {Karin E.} and Yawei Zhang and Vajdic, {Claire M.} and Wendy Cozen and Spinelli, {John J.} and Henrik Hjalgrim and Giles, {Graham G.} and Link, {Brian K.} and Jacqueline Clavel and Arslan, {Alan A.} and Purdue, {Mark P.} and Tinker, {Lesley F.} and Demetrius Albanes and Ferri, {Giovanni M.} and Habermann, {Thomas M.} and Adami, {Hans Olov} and Nikolaus Becker and Yolanda Benavente and Simonetta Bisanzi and Paolo Boffetta and Paul Brennan and Brooks-Wilson, {Angela R.} and Federico Canzian and Lucia Conde and Cox, {David G.} and Karen Curtin and Lenka Foretova and Gapstur, {Susan M.} and Herv{\'e} Ghesqui{\`e}res and Martha Glenn and Bengt Glimelius and Jackson, {Rebecca D.} and Qing Lan and Mark Liebow and Marc Maynadie and James McKay and Mads Melbye and Lucia Miligi and Milne, {Roger L.} and Molina, {Thierry J.} and Morton, {Lindsay M.} and North, {Kari E.} and Kenneth Offit and Marina Padoan and Patel, {Alpa V.} and Sara Piro and Vignesh Ravichandran and Elio Riboli and {de Sanjose}, Silvia and Severson, {Richard K.} and Southey, {Melissa C.} and Anthony Staines and Carolyn Stewart and Travis, {Ruth C.} and Elisabete Weiderpass and Stephanie Weinstein and Tongzhang Zheng and Chanock, {Stephen J.} and Nilanjan Chatterjee and Nathaniel Rothman and Birmann, {Brenda M.} and Cerhan, {James R.} and Berndt, {Sonja I.}",

note = "Funding Information: ATBC—The ATBC Study was supported by the Intramural Research Program of the U.S. National Cancer Institute, National Institutes of Health, and by U.S. Public Health Service contract HHSN261201500005C. Funding Information: PLCO—This research was supported by the Intramural Research Program of the National Cancer Institute and by contracts from the Division of Cancer Prevention, National Cancer Institute, NIH, DHHS. Funding Information: NHS (Meir J. Stampfer)—The NHS was supported in part by National Institutes of Health grants CA186107, CA87969, CA49449, CA149445, CA098122, and CA134958. We would like to thank the participants and staff of the Nurses{\textquoteright} Health Study for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. Funding Information: This work was supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute. Support for individual studies: Funding Information: UTAH/Sheffield—National Institutes of Health CA134674. Partial support for data collection at the Utah site was made possible by the Utah Population Database (UPDB) and the Utah Cancer Registry (UCR). Partial support for all datasets within the UPDB is provided by the Huntsman Cancer Institute (HCI) and the HCI Cancer Center Support grant, P30 CA42014. The UCR was supported in part by NIH contract HHSN261201000026C from the National Cancer Institute SEER Program with additional support from the Utah State Department of Health and the University of Utah. Partial support for data collection in Sheffield, UK was made possible by funds from Yorkshire Cancer Research and the Sheffield Experimental Cancer Medicine Centre. We thank the NCRI Haemato-oncology Clinical Studies Group, colleagues in the North Trent Cancer Network the North Trent Haemato-oncology Database. Funding Information: MSKCC—Geoffrey Beene Cancer Research Grant, Lymphoma Foundation (LF5541); Barbara K. Lipman Lymphoma Research Fund (74419); Robert and Kate Niehaus Clinical Cancer Genetics Research Initiative (57470). Funding Information: MCCS—The Melbourne Collaborative Cohort Study recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057, 251553, and 504711 and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry and the Australian Institute of Health and Welfare, including the National Death Index and the Australian Cancer Database. Funding Information: The authors thank Bill Wheeler, I.M.S., for assistance in performing some of the statistical analysis presented. Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization. Funding. Funding Information: GEC/Mayo GWAS—National Institutes of Health (CA118444, CA148690, CA92153). Intramural Research Program of the NIH, National Cancer Institute. Veterans Affairs Research Service. Data collection for Duke University was supported by a Leukemia & Lymphoma Society Career Development Award, the Bernstein Family Fund for Leukemia and Lymphoma Research, and the National Institutes of Health (K08CA134919), National Center for Advancing Translational Science (UL1 TR000135). Funding Information: HPFS (Walter C. Willet)—The HPFS was supported in part by National Institutes of Health grants CA167552, CA149445, and CA098122. We would like to thank the participants and staff of the Health Professionals Follow-up Study for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. Funding Information: UCSF2—The UCSF studies were supported by the NCI, National Institutes of Health, CA1046282 and CA154643. The collection of cancer incidence data used in this study was supported by the California Department of Health Services as part of the statewide cancer reporting program mandated by California Health and Safety Code section 103885; the National Cancer Institute{\textquoteright}s Surveillance, Epidemiology, and End Results Program under contract HHSN261201000140C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute; and the Centers for Disease Control and Prevention{\textquoteright}s National Program of Cancer Registries, under agreement #1U58 DP000807-01 awarded to the Public Health Institute. The ideas and opinions expressed herein are those of the authors, and endorsement by the State of California, the California Department of Health Services, the National Cancer Institute, or the Centers for Disease Control and Prevention or their contractors and subcontractors is not intended nor should be inferred. Funding Information: CPS-II—The Cancer Prevention Study-II (CPS-II) Nutrition Cohort was supported by the American Cancer Society. Genotyping for all CPS-II samples were supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The authors would also like to acknowledge the contribution to this study from central cancer registries supported through the Centers for Disease Control and Prevention National Program of Cancer Registries, and cancer registries supported by the National Cancer Institute Surveillance Epidemiology and End Results program. Funding Information: EpiLymph—European Commission (Grant references QLK4-CT-2000-00422 and FOOD-CT-2006-023103); the Spanish Ministry of Health (Grant references CIBERESP, PI11/01810, PI14/01219, RCESP C03/09, RTICESP C03/10 and RTIC RD06/0020/0095), the Marat{\'o} de TV3 Foundation (Grant reference 051210), the Ag{\`e}ncia de Gesti{\'o}d{\textquoteright}AjutsUniversitarisi de Recerca—Generalitat de Catalunya (Grant reference 2017SGR1085) who had no role in the data collection, analysis or interpretation of the results; the NIH (contract NO1-CO-12400); the Compagnia di San Paolo—Programma Oncologia; the Federal Office for Radiation Protection grants StSch4261 and StSch4420, the Jos{\'e} Carreras Leukemia Foundation grant DJCLS-R12/23, the German Federal Ministry for Education and Research (BMBF-01-EO-1303); the Health Research Board, Ireland and Cancer Research Ireland; Czech Republic supported by MH CZ—DRO (MMCI, 00209805) and MEYS-NPS ILO1413; Fondation de France and Association de Recherche Contre le Cancer. Funding Information: NSW—NSW was supported by grants from the Australian National Health and Medical Research Council (ID990920), the Cancer Council NSW, and the University of Sydney Faculty of Medicine. Funding Information: NCI-SEER—Intramural Research Program of the National Cancer Institute, National Institutes of Health, and Public Health Service (N01-PC-65064, N01-PC-67008, N01-PC-67009, N01-PC-67010, N02-PC-71105). Funding Information: SCALE—Swedish Cancer Society (2009/659). Stockholm County Council (20110209) and the Strategic Research Program in Epidemiology at Karolinska Institutet. Swedish Cancer Society grant (02 6661). National Institutes of Health (5R01 CA69669-02); Plan Denmark. Publisher Copyright: {\textcopyright} Copyright {\textcopyright} 2020 Moore, Kane, Wang, Panagiotou, Teras, Monnereau, Wong Doo, Machiela, Skibola, Slager, Salles, Camp, Bracci, Nieters, Vermeulen, Vijai, Smedby, Zhang, Vajdic, Cozen, Spinelli, Hjalgrim, Giles, Link, Clavel, Arslan, Purdue, Tinker, Albanes, Ferri, Habermann, Adami, Becker, Benavente, Bisanzi, Boffetta, Brennan, Brooks-Wilson, Canzian, Conde, Cox, Curtin, Foretova, Gapstur, Ghesqui{\`e}res, Glenn, Glimelius, Jackson, Lan, Liebow, Maynadie, McKay, Melbye, Miligi, Milne, Molina, Morton, North, Offit, Padoan, Patel, Piro, Ravichandran, Riboli, de Sanjose, Severson, Southey, Staines, Stewart, Travis, Weiderpass, Weinstein, Zheng, Chanock, Chatterjee, Rothman, Birmann, Cerhan and Berndt.",

year = "2020",

month = jan,

day = "28",

doi = "10.3389/fonc.2019.01539",

language = "English (US)",

volume = "9",

journal = "Frontiers in Oncology",

issn = "2234-943X",

publisher = "Frontiers Media S. A.",

}

TY - JOUR

T1 - Genetically Determined Height and Risk of Non-hodgkin Lymphoma

AU - Moore, Amy

AU - Kane, Eleanor

AU - Wang, Zhaoming

AU - Panagiotou, Orestis A.

AU - Teras, Lauren R.

AU - Monnereau, Alain

AU - Wong Doo, Nicole

AU - Machiela, Mitchell J.

AU - Skibola, Christine F.

AU - Slager, Susan L.

AU - Salles, Gilles

AU - Camp, Nicola J.

AU - Bracci, Paige M.

AU - Nieters, Alexandra

AU - Vermeulen, Roel C.H.

AU - Vijai, Joseph

AU - Smedby, Karin E.

AU - Zhang, Yawei

AU - Vajdic, Claire M.

AU - Cozen, Wendy

AU - Spinelli, John J.

AU - Hjalgrim, Henrik

AU - Giles, Graham G.

AU - Link, Brian K.

AU - Clavel, Jacqueline

AU - Arslan, Alan A.

AU - Purdue, Mark P.

AU - Tinker, Lesley F.

AU - Albanes, Demetrius

AU - Ferri, Giovanni M.

AU - Habermann, Thomas M.

AU - Adami, Hans Olov

AU - Becker, Nikolaus

AU - Benavente, Yolanda

AU - Bisanzi, Simonetta

AU - Boffetta, Paolo

AU - Brennan, Paul

AU - Brooks-Wilson, Angela R.

AU - Canzian, Federico

AU - Conde, Lucia

AU - Cox, David G.

AU - Curtin, Karen

AU - Foretova, Lenka

AU - Gapstur, Susan M.

AU - Ghesquières, Hervé

AU - Glenn, Martha

AU - Glimelius, Bengt

AU - Jackson, Rebecca D.

AU - Lan, Qing

AU - Liebow, Mark

AU - Maynadie, Marc

AU - McKay, James

AU - Melbye, Mads

AU - Miligi, Lucia

AU - Milne, Roger L.

AU - Molina, Thierry J.

AU - Morton, Lindsay M.

AU - North, Kari E.

AU - Offit, Kenneth

AU - Padoan, Marina

AU - Patel, Alpa V.

AU - Piro, Sara

AU - Ravichandran, Vignesh

AU - Riboli, Elio

AU - de Sanjose, Silvia

AU - Severson, Richard K.

AU - Southey, Melissa C.

AU - Staines, Anthony

AU - Stewart, Carolyn

AU - Travis, Ruth C.

AU - Weiderpass, Elisabete

AU - Weinstein, Stephanie

AU - Zheng, Tongzhang

AU - Chanock, Stephen J.

AU - Chatterjee, Nilanjan

AU - Rothman, Nathaniel

AU - Birmann, Brenda M.

AU - Cerhan, James R.

AU - Berndt, Sonja I.

N1 - Funding Information: ATBC—The ATBC Study was supported by the Intramural Research Program of the U.S. National Cancer Institute, National Institutes of Health, and by U.S. Public Health Service contract HHSN261201500005C. Funding Information: PLCO—This research was supported by the Intramural Research Program of the National Cancer Institute and by contracts from the Division of Cancer Prevention, National Cancer Institute, NIH, DHHS. Funding Information: NHS (Meir J. Stampfer)—The NHS was supported in part by National Institutes of Health grants CA186107, CA87969, CA49449, CA149445, CA098122, and CA134958. We would like to thank the participants and staff of the Nurses’ Health Study for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. Funding Information: This work was supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute. Support for individual studies: Funding Information: UTAH/Sheffield—National Institutes of Health CA134674. Partial support for data collection at the Utah site was made possible by the Utah Population Database (UPDB) and the Utah Cancer Registry (UCR). Partial support for all datasets within the UPDB is provided by the Huntsman Cancer Institute (HCI) and the HCI Cancer Center Support grant, P30 CA42014. The UCR was supported in part by NIH contract HHSN261201000026C from the National Cancer Institute SEER Program with additional support from the Utah State Department of Health and the University of Utah. Partial support for data collection in Sheffield, UK was made possible by funds from Yorkshire Cancer Research and the Sheffield Experimental Cancer Medicine Centre. We thank the NCRI Haemato-oncology Clinical Studies Group, colleagues in the North Trent Cancer Network the North Trent Haemato-oncology Database. Funding Information: MSKCC—Geoffrey Beene Cancer Research Grant, Lymphoma Foundation (LF5541); Barbara K. Lipman Lymphoma Research Fund (74419); Robert and Kate Niehaus Clinical Cancer Genetics Research Initiative (57470). Funding Information: MCCS—The Melbourne Collaborative Cohort Study recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057, 251553, and 504711 and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry and the Australian Institute of Health and Welfare, including the National Death Index and the Australian Cancer Database. Funding Information: The authors thank Bill Wheeler, I.M.S., for assistance in performing some of the statistical analysis presented. Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization. Funding. Funding Information: GEC/Mayo GWAS—National Institutes of Health (CA118444, CA148690, CA92153). Intramural Research Program of the NIH, National Cancer Institute. Veterans Affairs Research Service. Data collection for Duke University was supported by a Leukemia & Lymphoma Society Career Development Award, the Bernstein Family Fund for Leukemia and Lymphoma Research, and the National Institutes of Health (K08CA134919), National Center for Advancing Translational Science (UL1 TR000135). Funding Information: HPFS (Walter C. Willet)—The HPFS was supported in part by National Institutes of Health grants CA167552, CA149445, and CA098122. We would like to thank the participants and staff of the Health Professionals Follow-up Study for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. Funding Information: UCSF2—The UCSF studies were supported by the NCI, National Institutes of Health, CA1046282 and CA154643. The collection of cancer incidence data used in this study was supported by the California Department of Health Services as part of the statewide cancer reporting program mandated by California Health and Safety Code section 103885; the National Cancer Institute’s Surveillance, Epidemiology, and End Results Program under contract HHSN261201000140C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute; and the Centers for Disease Control and Prevention’s National Program of Cancer Registries, under agreement #1U58 DP000807-01 awarded to the Public Health Institute. The ideas and opinions expressed herein are those of the authors, and endorsement by the State of California, the California Department of Health Services, the National Cancer Institute, or the Centers for Disease Control and Prevention or their contractors and subcontractors is not intended nor should be inferred. Funding Information: CPS-II—The Cancer Prevention Study-II (CPS-II) Nutrition Cohort was supported by the American Cancer Society. Genotyping for all CPS-II samples were supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The authors would also like to acknowledge the contribution to this study from central cancer registries supported through the Centers for Disease Control and Prevention National Program of Cancer Registries, and cancer registries supported by the National Cancer Institute Surveillance Epidemiology and End Results program. Funding Information: EpiLymph—European Commission (Grant references QLK4-CT-2000-00422 and FOOD-CT-2006-023103); the Spanish Ministry of Health (Grant references CIBERESP, PI11/01810, PI14/01219, RCESP C03/09, RTICESP C03/10 and RTIC RD06/0020/0095), the Marató de TV3 Foundation (Grant reference 051210), the Agència de Gestiód’AjutsUniversitarisi de Recerca—Generalitat de Catalunya (Grant reference 2017SGR1085) who had no role in the data collection, analysis or interpretation of the results; the NIH (contract NO1-CO-12400); the Compagnia di San Paolo—Programma Oncologia; the Federal Office for Radiation Protection grants StSch4261 and StSch4420, the José Carreras Leukemia Foundation grant DJCLS-R12/23, the German Federal Ministry for Education and Research (BMBF-01-EO-1303); the Health Research Board, Ireland and Cancer Research Ireland; Czech Republic supported by MH CZ—DRO (MMCI, 00209805) and MEYS-NPS ILO1413; Fondation de France and Association de Recherche Contre le Cancer. Funding Information: NSW—NSW was supported by grants from the Australian National Health and Medical Research Council (ID990920), the Cancer Council NSW, and the University of Sydney Faculty of Medicine. Funding Information: NCI-SEER—Intramural Research Program of the National Cancer Institute, National Institutes of Health, and Public Health Service (N01-PC-65064, N01-PC-67008, N01-PC-67009, N01-PC-67010, N02-PC-71105). Funding Information: SCALE—Swedish Cancer Society (2009/659). Stockholm County Council (20110209) and the Strategic Research Program in Epidemiology at Karolinska Institutet. Swedish Cancer Society grant (02 6661). National Institutes of Health (5R01 CA69669-02); Plan Denmark. Publisher Copyright: © Copyright © 2020 Moore, Kane, Wang, Panagiotou, Teras, Monnereau, Wong Doo, Machiela, Skibola, Slager, Salles, Camp, Bracci, Nieters, Vermeulen, Vijai, Smedby, Zhang, Vajdic, Cozen, Spinelli, Hjalgrim, Giles, Link, Clavel, Arslan, Purdue, Tinker, Albanes, Ferri, Habermann, Adami, Becker, Benavente, Bisanzi, Boffetta, Brennan, Brooks-Wilson, Canzian, Conde, Cox, Curtin, Foretova, Gapstur, Ghesquières, Glenn, Glimelius, Jackson, Lan, Liebow, Maynadie, McKay, Melbye, Miligi, Milne, Molina, Morton, North, Offit, Padoan, Patel, Piro, Ravichandran, Riboli, de Sanjose, Severson, Southey, Staines, Stewart, Travis, Weiderpass, Weinstein, Zheng, Chanock, Chatterjee, Rothman, Birmann, Cerhan and Berndt.

PY - 2020/1/28

Y1 - 2020/1/28

N2 - Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00–1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01–1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.

AB - Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00–1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01–1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.

KW - chronic lymphocytic leukemia

KW - diffuse large B-cell lymphoma

KW - follicular lymphoma

KW - genetics

KW - height

KW - marginal zone lymphoma

KW - non-Hodgkin lymphoma

KW - polygenic risk score

UR - http://www.scopus.com/inward/record.url?scp=85079502127&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85079502127&partnerID=8YFLogxK

U2 - 10.3389/fonc.2019.01539

DO - 10.3389/fonc.2019.01539

M3 - Article

C2 - 32064237

AN - SCOPUS:85079502127

SN - 2234-943X

VL - 9

JO - Frontiers in Oncology

JF - Frontiers in Oncology

M1 - 1539

ER -

Genetically Determined Height and Risk of Non-hodgkin Lymphoma

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