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 | |
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
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In: Frontiers in Oncology, Vol. 9, 1539, 28.01.2020.
Research output: Contribution to journal › Article › peer-review
}
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 -