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Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

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Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups. / Urayama, Kevin Y.; Jarrett, Ruth F.; Hjalgrim, Henrik; Diepstra, Arjan; Kamatani, Yoichiro; Chabrier, Amelie; Gaborieau, Valerie; Boland, Anne; Nieters, Alexandra; Becker, Nikolaus; Foretova, Lenka; Benavente, Yolanda; Maynadié, Marc; Staines, Anthony; Shield, Lesley; Lake, Annette; Montgomery, Dorothy; Taylor, Malcolm; Smedby, Karin Ekström; Amini, Rose Marie; Adami, Hans Olov; Glimelius, Bengt; Feenstra, Bjarke; Nolte, Ilja M.; Visser, Lydia; Van Imhoff, Gustaaf W.; Lightfoot, Tracy; Cocco, Pierluigi; Kiemeney, Lambertus; Vermeulen, Sita H.; Holcatova, Ivana; Vatten, Lars; MacFarlane, Gary J.; Thomson, Peter; Conway, David I.; Benhamou, Simone; Agudo, Antonio; Healy, Claire M.; Overvad, Kim; Tjønneland, Anne; Melin, Beatrice; Canzian, Federico; Khaw, Kay Tee; Travis, Ruth C.; Peeters, Petra H.M.; González, Carlos A.; Quirós, José Ramón; Sánchez, María José; Huerta, José María; Melbye, Mads.

I: Journal of the National Cancer Institute, Bind 104, Nr. 3, 08.02.2012, s. 240-253.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Urayama, KY, Jarrett, RF, Hjalgrim, H, Diepstra, A, Kamatani, Y, Chabrier, A, Gaborieau, V, Boland, A, Nieters, A, Becker, N, Foretova, L, Benavente, Y, Maynadié, M, Staines, A, Shield, L, Lake, A, Montgomery, D, Taylor, M, Smedby, KE, Amini, RM, Adami, HO, Glimelius, B, Feenstra, B, Nolte, IM, Visser, L, Van Imhoff, GW, Lightfoot, T, Cocco, P, Kiemeney, L, Vermeulen, SH, Holcatova, I, Vatten, L, MacFarlane, GJ, Thomson, P, Conway, DI, Benhamou, S, Agudo, A, Healy, CM, Overvad, K, Tjønneland, A, Melin, B, Canzian, F, Khaw, KT, Travis, RC, Peeters, PHM, González, CA, Quirós, JR, Sánchez, MJ, Huerta, JM & Melbye, M 2012, 'Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups', Journal of the National Cancer Institute, bind 104, nr. 3, s. 240-253. https://doi.org/10.1093/jnci/djr516

APA

Urayama, K. Y., Jarrett, R. F., Hjalgrim, H., Diepstra, A., Kamatani, Y., Chabrier, A., Gaborieau, V., Boland, A., Nieters, A., Becker, N., Foretova, L., Benavente, Y., Maynadié, M., Staines, A., Shield, L., Lake, A., Montgomery, D., Taylor, M., Smedby, K. E., ... Melbye, M. (2012). Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups. Journal of the National Cancer Institute, 104(3), 240-253. https://doi.org/10.1093/jnci/djr516

Vancouver

Urayama KY, Jarrett RF, Hjalgrim H, Diepstra A, Kamatani Y, Chabrier A o.a. Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups. Journal of the National Cancer Institute. 2012 feb 8;104(3):240-253. https://doi.org/10.1093/jnci/djr516

Author

Urayama, Kevin Y. ; Jarrett, Ruth F. ; Hjalgrim, Henrik ; Diepstra, Arjan ; Kamatani, Yoichiro ; Chabrier, Amelie ; Gaborieau, Valerie ; Boland, Anne ; Nieters, Alexandra ; Becker, Nikolaus ; Foretova, Lenka ; Benavente, Yolanda ; Maynadié, Marc ; Staines, Anthony ; Shield, Lesley ; Lake, Annette ; Montgomery, Dorothy ; Taylor, Malcolm ; Smedby, Karin Ekström ; Amini, Rose Marie ; Adami, Hans Olov ; Glimelius, Bengt ; Feenstra, Bjarke ; Nolte, Ilja M. ; Visser, Lydia ; Van Imhoff, Gustaaf W. ; Lightfoot, Tracy ; Cocco, Pierluigi ; Kiemeney, Lambertus ; Vermeulen, Sita H. ; Holcatova, Ivana ; Vatten, Lars ; MacFarlane, Gary J. ; Thomson, Peter ; Conway, David I. ; Benhamou, Simone ; Agudo, Antonio ; Healy, Claire M. ; Overvad, Kim ; Tjønneland, Anne ; Melin, Beatrice ; Canzian, Federico ; Khaw, Kay Tee ; Travis, Ruth C. ; Peeters, Petra H.M. ; González, Carlos A. ; Quirós, José Ramón ; Sánchez, María José ; Huerta, José María ; Melbye, Mads. / Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups. I: Journal of the National Cancer Institute. 2012 ; Bind 104, Nr. 3. s. 240-253.

Bibtex

@article{97bd8d1e72ac4c4489a52cbd219e660e,
title = "Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups",
abstract = "Background Accumulating evidence suggests that risk factors for classical Hodgkin lymphoma (cHL) differ by tumor Epstein-Barr virus (EBV) status. This potential etiological heterogeneity is not recognized in current disease classification. Methods We conducted a genome-wide association study of 1200 cHL patients and 6417 control subjects, with validation in an independent replication series, to identify common genetic variants associated with total cHL and subtypes defined by tumor EBV status. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) assuming a log-additive genetic model for the variants. All statistical tests were two-sided. Results Two novel loci associated with total cHL irrespective of EBV status were identified in the major histocompatibility complex region; one resides adjacent to MICB (rs2248462: OR = 0.61, 95% CI = 0.53 to 0.69, P = 1.3 × 10 -13) and the other at HLA-DRA (rs2395185: OR = 0.56, 95% CI = 0.50 to 0.62, P = 8.3 × 10 -25) with both results confirmed in an independent replication series. Consistent with previous reports, associations were found between EBV-positive cHL and genetic variants within the class I region (rs2734986, HLA-A: OR = 2.45, 95% CI = 2.00 to 3.00, P = 1.2 × 10 -15; rs6904029, HCG9: OR = 0.46, 95% CI = 0.36 to 0.59, P = 5.5 × 10 -10) and between EBV-negative cHL and rs6903608 within the class II region (rs6903608, HLA-DRA: OR = 2.08, 95% CI = 1.84 to 2.35, P = 6.1 × 10 -31). The association between rs6903608 and EBV-negative cHL was confined to the nodular sclerosis histological subtype. Evidence for an association between EBV-negative cHL and rs20541 (5q31, IL13: OR = 1.53, 95% CI = 1.32 to 1.76, P = 5.4 x 10 -9), a variant previously linked to psoriasis and asthma, was observed; however, the evidence for replication was less clear. Notably, one additional psoriasis-associated variant, rs27524 (5q15, ERAP1), showed evidence of an association with cHL in the genome-wide association study (OR = 1.21, 95% CI = 1.10 to 1.33, P = 1.5 × 10 -4) and replication series (P =.03). Conclusion Overall, these results provide strong evidence that EBV status is an etiologically important classification of cHL and also suggest that some components of the pathological process are common to both EBV-positive and EBV-negative patients.",
author = "Urayama, {Kevin Y.} and Jarrett, {Ruth F.} and Henrik Hjalgrim and Arjan Diepstra and Yoichiro Kamatani and Amelie Chabrier and Valerie Gaborieau and Anne Boland and Alexandra Nieters and Nikolaus Becker and Lenka Foretova and Yolanda Benavente and Marc Maynadi{\'e} and Anthony Staines and Lesley Shield and Annette Lake and Dorothy Montgomery and Malcolm Taylor and Smedby, {Karin Ekstr{\"o}m} and Amini, {Rose Marie} and Adami, {Hans Olov} and Bengt Glimelius and Bjarke Feenstra and Nolte, {Ilja M.} and Lydia Visser and {Van Imhoff}, {Gustaaf W.} and Tracy Lightfoot and Pierluigi Cocco and Lambertus Kiemeney and Vermeulen, {Sita H.} and Ivana Holcatova and Lars Vatten and MacFarlane, {Gary J.} and Peter Thomson and Conway, {David I.} and Simone Benhamou and Antonio Agudo and Healy, {Claire M.} and Kim Overvad and Anne Tj{\o}nneland and Beatrice Melin and Federico Canzian and Khaw, {Kay Tee} and Travis, {Ruth C.} and Peeters, {Petra H.M.} and Gonz{\'a}lez, {Carlos A.} and Quir{\'o}s, {Jos{\'e} Ram{\'o}n} and S{\'a}nchez, {Mar{\'i}a Jos{\'e}} and Huerta, {Jos{\'e} Mar{\'i}a} and Mads Melbye",
year = "2012",
month = feb,
day = "8",
doi = "10.1093/jnci/djr516",
language = "English",
volume = "104",
pages = "240--253",
journal = "National Cancer Institute. Journal (Online)",
issn = "1460-2105",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Genome-wide association study of classical hodgkin lymphoma and epstein-barr virus status-defined subgroups

AU - Urayama, Kevin Y.

AU - Jarrett, Ruth F.

AU - Hjalgrim, Henrik

AU - Diepstra, Arjan

AU - Kamatani, Yoichiro

AU - Chabrier, Amelie

AU - Gaborieau, Valerie

AU - Boland, Anne

AU - Nieters, Alexandra

AU - Becker, Nikolaus

AU - Foretova, Lenka

AU - Benavente, Yolanda

AU - Maynadié, Marc

AU - Staines, Anthony

AU - Shield, Lesley

AU - Lake, Annette

AU - Montgomery, Dorothy

AU - Taylor, Malcolm

AU - Smedby, Karin Ekström

AU - Amini, Rose Marie

AU - Adami, Hans Olov

AU - Glimelius, Bengt

AU - Feenstra, Bjarke

AU - Nolte, Ilja M.

AU - Visser, Lydia

AU - Van Imhoff, Gustaaf W.

AU - Lightfoot, Tracy

AU - Cocco, Pierluigi

AU - Kiemeney, Lambertus

AU - Vermeulen, Sita H.

AU - Holcatova, Ivana

AU - Vatten, Lars

AU - MacFarlane, Gary J.

AU - Thomson, Peter

AU - Conway, David I.

AU - Benhamou, Simone

AU - Agudo, Antonio

AU - Healy, Claire M.

AU - Overvad, Kim

AU - Tjønneland, Anne

AU - Melin, Beatrice

AU - Canzian, Federico

AU - Khaw, Kay Tee

AU - Travis, Ruth C.

AU - Peeters, Petra H.M.

AU - González, Carlos A.

AU - Quirós, José Ramón

AU - Sánchez, María José

AU - Huerta, José María

AU - Melbye, Mads

PY - 2012/2/8

Y1 - 2012/2/8

N2 - Background Accumulating evidence suggests that risk factors for classical Hodgkin lymphoma (cHL) differ by tumor Epstein-Barr virus (EBV) status. This potential etiological heterogeneity is not recognized in current disease classification. Methods We conducted a genome-wide association study of 1200 cHL patients and 6417 control subjects, with validation in an independent replication series, to identify common genetic variants associated with total cHL and subtypes defined by tumor EBV status. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) assuming a log-additive genetic model for the variants. All statistical tests were two-sided. Results Two novel loci associated with total cHL irrespective of EBV status were identified in the major histocompatibility complex region; one resides adjacent to MICB (rs2248462: OR = 0.61, 95% CI = 0.53 to 0.69, P = 1.3 × 10 -13) and the other at HLA-DRA (rs2395185: OR = 0.56, 95% CI = 0.50 to 0.62, P = 8.3 × 10 -25) with both results confirmed in an independent replication series. Consistent with previous reports, associations were found between EBV-positive cHL and genetic variants within the class I region (rs2734986, HLA-A: OR = 2.45, 95% CI = 2.00 to 3.00, P = 1.2 × 10 -15; rs6904029, HCG9: OR = 0.46, 95% CI = 0.36 to 0.59, P = 5.5 × 10 -10) and between EBV-negative cHL and rs6903608 within the class II region (rs6903608, HLA-DRA: OR = 2.08, 95% CI = 1.84 to 2.35, P = 6.1 × 10 -31). The association between rs6903608 and EBV-negative cHL was confined to the nodular sclerosis histological subtype. Evidence for an association between EBV-negative cHL and rs20541 (5q31, IL13: OR = 1.53, 95% CI = 1.32 to 1.76, P = 5.4 x 10 -9), a variant previously linked to psoriasis and asthma, was observed; however, the evidence for replication was less clear. Notably, one additional psoriasis-associated variant, rs27524 (5q15, ERAP1), showed evidence of an association with cHL in the genome-wide association study (OR = 1.21, 95% CI = 1.10 to 1.33, P = 1.5 × 10 -4) and replication series (P =.03). Conclusion Overall, these results provide strong evidence that EBV status is an etiologically important classification of cHL and also suggest that some components of the pathological process are common to both EBV-positive and EBV-negative patients.

AB - Background Accumulating evidence suggests that risk factors for classical Hodgkin lymphoma (cHL) differ by tumor Epstein-Barr virus (EBV) status. This potential etiological heterogeneity is not recognized in current disease classification. Methods We conducted a genome-wide association study of 1200 cHL patients and 6417 control subjects, with validation in an independent replication series, to identify common genetic variants associated with total cHL and subtypes defined by tumor EBV status. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) assuming a log-additive genetic model for the variants. All statistical tests were two-sided. Results Two novel loci associated with total cHL irrespective of EBV status were identified in the major histocompatibility complex region; one resides adjacent to MICB (rs2248462: OR = 0.61, 95% CI = 0.53 to 0.69, P = 1.3 × 10 -13) and the other at HLA-DRA (rs2395185: OR = 0.56, 95% CI = 0.50 to 0.62, P = 8.3 × 10 -25) with both results confirmed in an independent replication series. Consistent with previous reports, associations were found between EBV-positive cHL and genetic variants within the class I region (rs2734986, HLA-A: OR = 2.45, 95% CI = 2.00 to 3.00, P = 1.2 × 10 -15; rs6904029, HCG9: OR = 0.46, 95% CI = 0.36 to 0.59, P = 5.5 × 10 -10) and between EBV-negative cHL and rs6903608 within the class II region (rs6903608, HLA-DRA: OR = 2.08, 95% CI = 1.84 to 2.35, P = 6.1 × 10 -31). The association between rs6903608 and EBV-negative cHL was confined to the nodular sclerosis histological subtype. Evidence for an association between EBV-negative cHL and rs20541 (5q31, IL13: OR = 1.53, 95% CI = 1.32 to 1.76, P = 5.4 x 10 -9), a variant previously linked to psoriasis and asthma, was observed; however, the evidence for replication was less clear. Notably, one additional psoriasis-associated variant, rs27524 (5q15, ERAP1), showed evidence of an association with cHL in the genome-wide association study (OR = 1.21, 95% CI = 1.10 to 1.33, P = 1.5 × 10 -4) and replication series (P =.03). Conclusion Overall, these results provide strong evidence that EBV status is an etiologically important classification of cHL and also suggest that some components of the pathological process are common to both EBV-positive and EBV-negative patients.

UR - http://www.scopus.com/inward/record.url?scp=84856845730&partnerID=8YFLogxK

U2 - 10.1093/jnci/djr516

DO - 10.1093/jnci/djr516

M3 - Journal article

C2 - 22286212

AN - SCOPUS:84856845730

VL - 104

SP - 240

EP - 253

JO - National Cancer Institute. Journal (Online)

JF - National Cancer Institute. Journal (Online)

SN - 1460-2105

IS - 3

ER -

ID: 258216059