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

Research output: Contribution to journalArticle

1 Citation (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.

Original languageEnglish (US)
Pages (from-to)844-863
Number of pages20
JournalGenetic epidemiology
Volume43
Issue number7
DOIs
StatePublished - Oct 1 2019

Fingerprint

Non-Hodgkin's Lymphoma
Autoimmune Diseases
Genome-Wide Association Study
Meta-Analysis
Follicular Lymphoma
Lymphoma, Large B-Cell, Diffuse
Telomere
B-Cell Chronic Lymphocytic Leukemia
Systemic Lupus Erythematosus
Sample Size
Multiple Sclerosis
Epidemiologic Studies
Lymphoma
Rheumatoid Arthritis
Apoptosis
Inflammation
Antigens
Genes
Neoplasms

Keywords

  • autoimmune disease
  • genome-wide association study
  • meta-analysis
  • non-Hodgkin lymphoma

ASJC Scopus subject areas

  • Epidemiology
  • Genetics(clinical)

Cite this

Din, L., Sheikh, M., Kosaraju, N., Smedby, K. E., Bernatsky, S., Berndt, S. I., ... 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

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

In: Genetic epidemiology, Vol. 43, No. 7, 01.10.2019, p. 844-863.

Research output: Contribution to journalArticle

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, vol. 43, no. 7, pp. 844-863. https://doi.org/10.1002/gepi.22242
Din L, Sheikh M, Kosaraju N, Smedby KE, Bernatsky S, Berndt SI et al. Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes. Genetic epidemiology. 2019 Oct 1;43(7):844-863. https://doi.org/10.1002/gepi.22242
Din, Lennox ; Sheikh, Mohammad ; Kosaraju, Nikitha ; Smedby, Karin Ekstrom ; Bernatsky, Sasha ; Berndt, Sonja I. ; Skibola, Christine F. ; Nieters, Alexandra ; Wang, Sophia ; McKay, James D. ; Cocco, Pierluigi ; Maynadié, Marc ; Foretová, Lenka ; Staines, Anthony ; Mack, Thomas M. ; de Sanjosé, Silvia ; Vyse, Timothy J. ; Padyukov, Leonid ; Monnereau, Alain ; Arslan, Alan A. ; Moore, Amy ; Brooks-Wilson, Angela R. ; Novak, Anne J. ; Glimelius, Bengt ; Birmann, Brenda M. ; Link, Brian K. ; Stewart, Carolyn ; Vajdic, Claire M. ; Haioun, Corinne ; Magnani, Corrado ; Conti, David V. ; Cox, David G. ; Casabonne, Delphine ; Albanes, Demetrius ; Kane, Eleanor ; Roman, Eve ; Muzi, Giacomo ; Salles, Gilles ; Giles, Graham G. ; Adami, Hans Olov ; Ghesquières, Hervé ; De Vivo, Immaculata ; Clavel, Jacqueline ; Cerhan, James R. ; Spinelli, John J. ; Hofmann, Jonathan ; Vijai, Joseph ; Curtin, Karen ; Costenbader, Karen H. ; Onel, Kenan ; Offit, Kenneth ; Teras, Lauren R. ; Morton, Lindsay ; Conde, Lucia ; Miligi, Lucia ; Melbye, Mads ; Ennas, Maria Grazia ; Liebow, Mark ; Purdue, Mark P. ; Glenn, Martha ; Southey, Melissa C. ; Din, Morris ; Rothman, Nathaniel ; Camp, Nicola J. ; Wong Doo, Nicole ; Becker, Nikolaus ; Pradhan, Nisha ; Bracci, Paige M. ; Boffetta, Paolo ; Vineis, Paolo ; Brennan, Paul ; Kraft, Peter ; Lan, Qing ; Severson, Richard K. ; Vermeulen, Roel C.H. ; Milne, Roger L. ; Kaaks, Rudolph ; Travis, Ruth C. ; Weinstein, Stephanie J. ; Chanock, Stephen J. ; Ansell, Stephen M. ; Slager, Susan L. ; Zheng, Tongzhang ; Zhang, Yawei ; Benavente, Yolanda ; Taub, Zachary ; Madireddy, Lohith ; Gourraud, Pierre Antoine ; Oksenberg, Jorge R. ; Cozen, Wendy ; Hjalgrim, Henrik ; Khankhanian, Pouya. / Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes. In: Genetic epidemiology. 2019 ; Vol. 43, No. 7. pp. 844-863.
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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.",
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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 - 2019/10/1

Y1 - 2019/10/1

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

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