Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

Lennox Din; Mohammad Sheikh; Nikitha Kosaraju; Karin Ekstrom Smedby; Sasha Bernatsky; Sonja I. Berndt; Christine F. Skibola; Alexandra Nieters; Sophia Wang; James D. McKay; Pierluigi Cocco; Marc Maynadié; Lenka Foretová; Anthony Staines; Thomas M. Mack; Silvia de Sanjosé; Timothy J. Vyse; Leonid Padyukov; Alain Monnereau; Alan A. Arslan; Amy Moore; Angela R. Brooks-Wilson; Anne J. Novak; Bengt Glimelius; Brenda M. Birmann; Brian K. Link; Carolyn Stewart; Claire M. Vajdic; Corinne Haioun; Corrado Magnani; David V. Conti; David G. Cox; Delphine Casabonne; Demetrius Albanes; Eleanor Kane; Eve Roman; Giacomo Muzi; Gilles Salles; Graham G. Giles; Hans Olov Adami; Hervé Ghesquières; Immaculata De Vivo; Jacqueline Clavel; James R. Cerhan; John J. Spinelli; Jonathan Hofmann; Joseph Vijai; Karen Curtin; Karen H. Costenbader; Kenan Onel; Kenneth Offit; Lauren R. Teras; Lindsay Morton; Lucia Conde; Lucia Miligi; Mads Melbye; Maria Grazia Ennas; Mark Liebow; Mark P. Purdue; Martha Glenn; Melissa C. Southey; Morris Din; Nathaniel Rothman; Nicola J. Camp; Nicole Wong Doo; Nikolaus Becker; Nisha Pradhan; Paige M. Bracci; Paolo Boffetta; Paolo Vineis; Paul Brennan; Peter Kraft; Qing Lan; Richard K. Severson; Roel C.H. Vermeulen; Roger L. Milne; Rudolph Kaaks; Ruth C. Travis; Stephanie J. Weinstein; Stephen J. Chanock; Stephen M. Ansell; Susan L. Slager; Tongzhang Zheng; Yawei Zhang; Yolanda Benavente; Zachary Taub; Lohith Madireddy; Pierre Antoine Gourraud; Jorge R. Oksenberg; Wendy Cozen; Henrik Hjalgrim; Pouya Khankhanian

doi:10.1002/gepi.22242

Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

Lennox Din, Mohammad Sheikh, Nikitha Kosaraju, Karin Ekstrom Smedby, Sasha Bernatsky, Sonja I. Berndt, Christine F. Skibola, Alexandra Nieters, Sophia Wang, James D. McKay, Pierluigi Cocco, Marc Maynadié, Lenka Foretová, Anthony Staines, Thomas M. Mack, Silvia de Sanjosé, Timothy J. Vyse, Leonid Padyukov, Alain Monnereau, Alan A. ArslanAmy Moore, Angela R. Brooks-Wilson, Anne J. Novak, Bengt Glimelius, Brenda M. Birmann, Brian K. Link, Carolyn Stewart, Claire M. Vajdic, Corinne Haioun, Corrado Magnani, David V. Conti, David G. Cox, Delphine Casabonne, Demetrius Albanes, Eleanor Kane, Eve Roman, Giacomo Muzi, Gilles Salles, Graham G. Giles, Hans Olov Adami, Hervé Ghesquières, Immaculata De Vivo, Jacqueline Clavel, James R. Cerhan, John J. Spinelli, Jonathan Hofmann, Joseph Vijai, Karen Curtin, Karen H. Costenbader, Kenan Onel, Kenneth Offit, Lauren R. Teras, Lindsay Morton, Lucia Conde, Lucia Miligi, Mads Melbye, Maria Grazia Ennas, Mark Liebow, Mark P. Purdue, Martha Glenn, Melissa C. Southey, Morris Din, Nathaniel Rothman, Nicola J. Camp, Nicole Wong Doo, Nikolaus Becker, Nisha Pradhan, Paige M. Bracci, Paolo Boffetta, Paolo Vineis, Paul Brennan, Peter Kraft, Qing Lan, Richard K. Severson, Roel C.H. Vermeulen, Roger L. Milne, Rudolph Kaaks, Ruth C. Travis, Stephanie J. Weinstein, Stephen J. Chanock, Stephen M. Ansell, Susan L. Slager, Tongzhang Zheng, Yawei Zhang, Yolanda Benavente, Zachary Taub, Lohith Madireddy, Pierre Antoine Gourraud, Jorge R. Oksenberg, Wendy Cozen, Henrik Hjalgrim, Pouya Khankhanian^*

^*Corresponding author af dette arbejde

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

28 Citationer (Scopus)

Abstract

Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p =.0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.

Originalsprog	Engelsk
Tidsskrift	Genetic Epidemiology
Vol/bind	43
Udgave nummer	7
Sider (fra-til)	844-863
Antal sider	20
ISSN	0741-0395
DOI	https://doi.org/10.1002/gepi.22242
Status	Udgivet - 2019
Udgivet eksternt	Ja

Adgang til dokumentet

10.1002/gepi.22242

Citationsformater

Din, L., Sheikh, M., Kosaraju, N., Smedby, K. E., Bernatsky, S., Berndt, S. I., Skibola, C. F., Nieters, A., Wang, S., McKay, J. D., Cocco, P., Maynadié, M., Foretová, L., Staines, A., Mack, T. M., de Sanjosé, S., Vyse, T. J., Padyukov, L., Monnereau, A., ... Khankhanian, P. (2019). Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes. Genetic Epidemiology, 43(7), 844-863. https://doi.org/10.1002/gepi.22242

Din, L, Sheikh, M, Kosaraju, N, Smedby, KE, Bernatsky, S, Berndt, SI, Skibola, CF, Nieters, A, Wang, S, McKay, JD, Cocco, P, Maynadié, M, Foretová, L, Staines, A, Mack, TM, de Sanjosé, S, Vyse, TJ, Padyukov, L, Monnereau, A, Arslan, AA, Moore, A, Brooks-Wilson, AR, Novak, AJ, Glimelius, B, Birmann, BM, Link, BK, Stewart, C, Vajdic, CM, Haioun, C, Magnani, C, Conti, DV, Cox, DG, Casabonne, D, Albanes, D, Kane, E, Roman, E, Muzi, G, Salles, G, Giles, GG, Adami, HO, Ghesquières, H, De Vivo, I, Clavel, J, Cerhan, JR, Spinelli, JJ, Hofmann, J, Vijai, J, Curtin, K, Costenbader, KH, Onel, K, Offit, K, Teras, LR, Morton, L, Conde, L, Miligi, L, Melbye, M, Ennas, MG, Liebow, M, Purdue, MP, Glenn, M, Southey, MC, Din, M, Rothman, N, Camp, NJ, Wong Doo, N, Becker, N, Pradhan, N, Bracci, PM, Boffetta, P, Vineis, P, Brennan, P, Kraft, P, Lan, Q, Severson, RK, Vermeulen, RCH, Milne, RL, Kaaks, R, Travis, RC, Weinstein, SJ, Chanock, SJ, Ansell, SM, Slager, SL, Zheng, T, Zhang, Y, Benavente, Y, Taub, Z, Madireddy, L, Gourraud, PA, Oksenberg, JR, Cozen, W, Hjalgrim, H & Khankhanian, P 2019, 'Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes', Genetic Epidemiology, bind 43, nr. 7, s. 844-863. https://doi.org/10.1002/gepi.22242

@article{6bdabe78357445e89b62469cb692a45d,

title = "Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes",

abstract = "Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c){"}diseasome{"}, (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p =.0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.",

keywords = "autoimmune disease, genome-wide association study, meta-analysis, non-Hodgkin lymphoma",

author = "Lennox Din and Mohammad Sheikh and Nikitha Kosaraju and Smedby, {Karin Ekstrom} and Sasha Bernatsky and Berndt, {Sonja I.} and Skibola, {Christine F.} and Alexandra Nieters and Sophia Wang and McKay, {James D.} and Pierluigi Cocco and Marc Maynadi{\'e} and Lenka Foretov{\'a} and Anthony Staines and Mack, {Thomas M.} and {de Sanjos{\'e}}, Silvia and Vyse, {Timothy J.} and Leonid Padyukov and Alain Monnereau and Arslan, {Alan A.} and Amy Moore and Brooks-Wilson, {Angela R.} and Novak, {Anne J.} and Bengt Glimelius and Birmann, {Brenda M.} and Link, {Brian K.} and Carolyn Stewart and Vajdic, {Claire M.} and Corinne Haioun and Corrado Magnani and Conti, {David V.} and Cox, {David G.} and Delphine Casabonne and Demetrius Albanes and Eleanor Kane and Eve Roman and Giacomo Muzi and Gilles Salles and Giles, {Graham G.} and Adami, {Hans Olov} and Herv{\'e} Ghesqui{\`e}res and {De Vivo}, Immaculata and Jacqueline Clavel and Cerhan, {James R.} and Spinelli, {John J.} and Jonathan Hofmann and Joseph Vijai and Karen Curtin and Costenbader, {Karen H.} and Kenan Onel and Kenneth Offit and Teras, {Lauren R.} and Lindsay Morton and Lucia Conde and Lucia Miligi and Mads Melbye and Ennas, {Maria Grazia} and Mark Liebow and Purdue, {Mark P.} and Martha Glenn and Southey, {Melissa C.} and Morris Din and Nathaniel Rothman and Camp, {Nicola J.} and {Wong Doo}, Nicole and Nikolaus Becker and Nisha Pradhan and Bracci, {Paige M.} and Paolo Boffetta and Paolo Vineis and Paul Brennan and Peter Kraft and Qing Lan and Severson, {Richard K.} and Vermeulen, {Roel C.H.} and Milne, {Roger L.} and Rudolph Kaaks and Travis, {Ruth C.} and Weinstein, {Stephanie J.} and Chanock, {Stephen J.} and Ansell, {Stephen M.} and Slager, {Susan L.} and Tongzhang Zheng and Yawei Zhang and Yolanda Benavente and Zachary Taub and Lohith Madireddy and Gourraud, {Pierre Antoine} and Oksenberg, {Jorge R.} and Wendy Cozen and Henrik Hjalgrim and Pouya Khankhanian",

year = "2019",

doi = "10.1002/gepi.22242",

language = "English",

volume = "43",

pages = "844--863",

journal = "Genetic Epidemiology",

issn = "0741-0395",

publisher = "JohnWiley & Sons, Inc.",

number = "7",

}

TY - JOUR

T1 - Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

AU - Din, Lennox

AU - Sheikh, Mohammad

AU - Kosaraju, Nikitha

AU - Smedby, Karin Ekstrom

AU - Bernatsky, Sasha

AU - Berndt, Sonja I.

AU - Skibola, Christine F.

AU - Nieters, Alexandra

AU - Wang, Sophia

AU - McKay, James D.

AU - Cocco, Pierluigi

AU - Maynadié, Marc

AU - Foretová, Lenka

AU - Staines, Anthony

AU - Mack, Thomas M.

AU - de Sanjosé, Silvia

AU - Vyse, Timothy J.

AU - Padyukov, Leonid

AU - Monnereau, Alain

AU - Arslan, Alan A.

AU - Moore, Amy

AU - Brooks-Wilson, Angela R.

AU - Novak, Anne J.

AU - Glimelius, Bengt

AU - Birmann, Brenda M.

AU - Link, Brian K.

AU - Stewart, Carolyn

AU - Vajdic, Claire M.

AU - Haioun, Corinne

AU - Magnani, Corrado

AU - Conti, David V.

AU - Cox, David G.

AU - Casabonne, Delphine

AU - Albanes, Demetrius

AU - Kane, Eleanor

AU - Roman, Eve

AU - Muzi, Giacomo

AU - Salles, Gilles

AU - Giles, Graham G.

AU - Adami, Hans Olov

AU - Ghesquières, Hervé

AU - De Vivo, Immaculata

AU - Clavel, Jacqueline

AU - Cerhan, James R.

AU - Spinelli, John J.

AU - Hofmann, Jonathan

AU - Vijai, Joseph

AU - Curtin, Karen

AU - Costenbader, Karen H.

AU - Onel, Kenan

AU - Offit, Kenneth

AU - Teras, Lauren R.

AU - Morton, Lindsay

AU - Conde, Lucia

AU - Miligi, Lucia

AU - Melbye, Mads

AU - Ennas, Maria Grazia

AU - Liebow, Mark

AU - Purdue, Mark P.

AU - Glenn, Martha

AU - Southey, Melissa C.

AU - Din, Morris

AU - Rothman, Nathaniel

AU - Camp, Nicola J.

AU - Wong Doo, Nicole

AU - Becker, Nikolaus

AU - Pradhan, Nisha

AU - Bracci, Paige M.

AU - Boffetta, Paolo

AU - Vineis, Paolo

AU - Brennan, Paul

AU - Kraft, Peter

AU - Lan, Qing

AU - Severson, Richard K.

AU - Vermeulen, Roel C.H.

AU - Milne, Roger L.

AU - Kaaks, Rudolph

AU - Travis, Ruth C.

AU - Weinstein, Stephanie J.

AU - Chanock, Stephen J.

AU - Ansell, Stephen M.

AU - Slager, Susan L.

AU - Zheng, Tongzhang

AU - Zhang, Yawei

AU - Benavente, Yolanda

AU - Taub, Zachary

AU - Madireddy, Lohith

AU - Gourraud, Pierre Antoine

AU - Oksenberg, Jorge R.

AU - Cozen, Wendy

AU - Hjalgrim, Henrik

AU - Khankhanian, Pouya

PY - 2019

Y1 - 2019

N2 - Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p =.0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.

AB - Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p =.0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.

KW - autoimmune disease

KW - genome-wide association study

KW - meta-analysis

KW - non-Hodgkin lymphoma

U2 - 10.1002/gepi.22242

DO - 10.1002/gepi.22242

M3 - Journal article

C2 - 31407831

AN - SCOPUS:85070768686

SN - 0741-0395

VL - 43

SP - 844

EP - 863

JO - Genetic Epidemiology

JF - Genetic Epidemiology

IS - 7

ER -