Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

L. Din; M. Sheikh; N. Kosaraju; K.E. Smedby; S. Bernatsky; S.I. Berndt; C.F. Skibola; A. Nieters; J.D. McKay; P. Cocco; M. Maynadié; L. Foretová; A. Staines; T.M. Mack; S. de Sanjosé; T.J. Vyse; L. Padyukov; A. Monnereau; A.A. Arslan; A. Moore; A.R. Brooks-Wilson; B. Glimelius; B.M. Birmann; B.K. Link; C. Stewart; C.M. Vajdic; C. Haioun; C. Magnani; D.V. Conti; D.G. Cox; D. Casabonne; D. Albanes; E. Kane; E. Roman; G. Muzi; G. Salles; G.G. Giles; H.-O. Adami; H. Ghesquières; I. De Vivo; J. Clavel; J.R. Cerhan; J.J. Spinelli; J. Vijai; K. Curtin; K.H. Costenbader; K. Onel; K. Offit; L.R. Teras; L. Morton; L. Conde; L. Miligi; M. Melbye; M.G. Ennas; M. Liebow; M.P. Purdue; M. Glenn; M.C. Southey; M. Din; N. Rothman; N.J. Camp; N. Wong Doo; N. Becker; N. Pradhan; P.M. Bracci; P. Boffetta; P. Vineis; P. Brennan; P. Kraft; Q. Lan; R.K. Severson; R.C.H. Vermeulen; R.L. Milne; R. Kaaks; R.C. Travis; S.J. Weinstein; S.J. Chanock; S.M. Ansell; S.L. Slager; T. Zheng; Y. Benavente; Z. Taub; L. Madireddy; P.-A. Gourraud; J.R. Oksenberg; W. Cozen; H. Hjalgrim; P. Khankhanian

doi:10.1002/gepi.22242

Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

L. Din, M. Sheikh, N. Kosaraju, K.E. Smedby, S. Bernatsky, S.I. Berndt, C.F. Skibola, A. Nieters, J.D. McKay, P. Cocco, M. Maynadié, L. Foretová, A. Staines, T.M. Mack, S. de Sanjosé, T.J. Vyse, L. Padyukov, A. Monnereau, A.A. Arslan, A. MooreA.R. Brooks-Wilson, B. Glimelius, B.M. Birmann, B.K. Link, C. Stewart, C.M. Vajdic, C. Haioun, C. Magnani, D.V. Conti, D.G. Cox, D. Casabonne, D. Albanes, E. Kane, E. Roman, G. Muzi, G. Salles, G.G. Giles, H.-O. Adami, H. Ghesquières, I. De Vivo, J. Clavel, J.R. Cerhan, J.J. Spinelli, J. Vijai, K. Curtin, K.H. Costenbader, K. Onel, K. Offit, L.R. Teras, L. Morton, L. Conde, L. Miligi, M. Melbye, M.G. Ennas, M. Liebow, M.P. Purdue, M. Glenn, M.C. Southey, M. Din, N. Rothman, N.J. Camp, N. Wong Doo, N. Becker, N. Pradhan, P.M. Bracci, P. Boffetta, P. Vineis, P. Brennan, P. Kraft, Q. Lan, R.K. Severson, R.C.H. Vermeulen, R.L. Milne, R. Kaaks, R.C. Travis, S.J. Weinstein, S.J. Chanock, S.M. Ansell, S.L. Slager, T. Zheng, Y. Benavente, Z. Taub, L. Madireddy, P.-A. Gourraud, J.R. Oksenberg, W. Cozen, H. Hjalgrim, P. Khankhanian

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

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 language	English
Pages (from-to)	844-863
Number of pages	20
Journal	Genetic Epidemiology
Volume	43
Issue number	7
DOIs	https://doi.org/10.1002/gepi.22242
Publication status	Published - 2019

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10.1002/gepi.22242

Genetic Epidemiology - 2019 - Din - Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypesFinal published version, 1.06 MBLicence: Taverne

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Din, L., Sheikh, M., Kosaraju, N., Smedby, K. E., Bernatsky, S., Berndt, S. I., Skibola, C. F., Nieters, A., McKay, J. D., Cocco, P., Maynadié, M., Foretová, L., Staines, A., Mack, T. M., de Sanjosé, S., Vyse, T. J., Padyukov, L., Monnereau, A., Arslan, A. 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

@article{ace2a7c648a349a2b9457d2104054fa8,

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.",

author = "L. Din and M. Sheikh and N. Kosaraju and K.E. Smedby and S. Bernatsky and S.I. Berndt and C.F. Skibola and A. Nieters and J.D. McKay and P. Cocco and M. Maynadi{\'e} and L. Foretov{\'a} and A. Staines and T.M. Mack and {de Sanjos{\'e}}, S. and T.J. Vyse and L. Padyukov and A. Monnereau and A.A. Arslan and A. Moore and A.R. Brooks-Wilson and B. Glimelius and B.M. Birmann and B.K. Link and C. Stewart and C.M. Vajdic and C. Haioun and C. Magnani and D.V. Conti and D.G. Cox and D. Casabonne and D. Albanes and E. Kane and E. Roman and G. Muzi and G. Salles and G.G. Giles and H.-O. Adami and H. Ghesqui{\`e}res and {De Vivo}, I. and J. Clavel and J.R. Cerhan and J.J. Spinelli and J. Vijai and K. Curtin and K.H. Costenbader and K. Onel and K. Offit and L.R. Teras and L. Morton and L. Conde and L. Miligi and M. Melbye and M.G. Ennas and M. Liebow and M.P. Purdue and M. Glenn and M.C. Southey and M. Din and N. Rothman and N.J. Camp and {Wong Doo}, N. and N. Becker and N. Pradhan and P.M. Bracci and P. Boffetta and P. Vineis and P. Brennan and P. Kraft and Q. Lan and R.K. Severson and R.C.H. Vermeulen and R.L. Milne and R. Kaaks and R.C. Travis and S.J. Weinstein and S.J. Chanock and S.M. Ansell and S.L. Slager and T. Zheng and Y. Benavente and Z. Taub and L. Madireddy and P.-A. Gourraud and J.R. Oksenberg and W. Cozen and H. Hjalgrim and P. Khankhanian",

note = "Cited By :12 Export Date: 8 December 2021",

year = "2019",

doi = "10.1002/gepi.22242",

language = "English",

volume = "43",

pages = "844--863",

journal = "Genetic Epidemiology",

issn = "0741-0395",

publisher = "Wiley-Liss Inc.",

number = "7",

}

Din, L, Sheikh, M, Kosaraju, N, Smedby, KE, Bernatsky, S, Berndt, SI, Skibola, CF, Nieters, A, 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, 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, H-O, Ghesquières, H, De Vivo, I, Clavel, J, Cerhan, JR, Spinelli, JJ, 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, Benavente, Y, Taub, Z, Madireddy, L, Gourraud, P-A, 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

TY - JOUR

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

AU - Din, L.

AU - Sheikh, M.

AU - Kosaraju, N.

AU - Smedby, K.E.

AU - Bernatsky, S.

AU - Berndt, S.I.

AU - Skibola, C.F.

AU - Nieters, A.

AU - McKay, J.D.

AU - Cocco, P.

AU - Maynadié, M.

AU - Foretová, L.

AU - Staines, A.

AU - Mack, T.M.

AU - de Sanjosé, S.

AU - Vyse, T.J.

AU - Padyukov, L.

AU - Monnereau, A.

AU - Arslan, A.A.

AU - Moore, A.

AU - Brooks-Wilson, A.R.

AU - Glimelius, B.

AU - Birmann, B.M.

AU - Link, B.K.

AU - Stewart, C.

AU - Vajdic, C.M.

AU - Haioun, C.

AU - Magnani, C.

AU - Conti, D.V.

AU - Cox, D.G.

AU - Casabonne, D.

AU - Albanes, D.

AU - Kane, E.

AU - Roman, E.

AU - Muzi, G.

AU - Salles, G.

AU - Giles, G.G.

AU - Adami, H.-O.

AU - Ghesquières, H.

AU - De Vivo, I.

AU - Clavel, J.

AU - Cerhan, J.R.

AU - Spinelli, J.J.

AU - Vijai, J.

AU - Curtin, K.

AU - Costenbader, K.H.

AU - Onel, K.

AU - Offit, K.

AU - Teras, L.R.

AU - Morton, L.

AU - Conde, L.

AU - Miligi, L.

AU - Melbye, M.

AU - Ennas, M.G.

AU - Liebow, M.

AU - Purdue, M.P.

AU - Glenn, M.

AU - Southey, M.C.

AU - Din, M.

AU - Rothman, N.

AU - Camp, N.J.

AU - Wong Doo, N.

AU - Becker, N.

AU - Pradhan, N.

AU - Bracci, P.M.

AU - Boffetta, P.

AU - Vineis, P.

AU - Brennan, P.

AU - Kraft, P.

AU - Lan, Q.

AU - Severson, R.K.

AU - Vermeulen, R.C.H.

AU - Milne, R.L.

AU - Kaaks, R.

AU - Travis, R.C.

AU - Weinstein, S.J.

AU - Chanock, S.J.

AU - Ansell, S.M.

AU - Slager, S.L.

AU - Zheng, T.

AU - Benavente, Y.

AU - Taub, Z.

AU - Madireddy, L.

AU - Gourraud, P.-A.

AU - Oksenberg, J.R.

AU - Cozen, W.

AU - Hjalgrim, H.

AU - Khankhanian, P.

N1 - Cited By :12 Export Date: 8 December 2021

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.

U2 - 10.1002/gepi.22242

DO - 10.1002/gepi.22242

M3 - Article

SN - 0741-0395

VL - 43

SP - 844

EP - 863

JO - Genetic Epidemiology

JF - Genetic Epidemiology

IS - 7

ER -

Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

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