Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma

Bernatsky, Sasha; García, Héctor Alexander Velásquez; Spinelli, John J.; Gaffney, Patrick M.; Smedby, Karin E.; Ramsey‐Goldman, Rosalind; Wang, Sophia; Adami, Hans Olov; Albanês, Demetrius; Angelucci, Emanuele; Ansell, Stephen M.; Asmann, Yan W.; Becker, Nikolaus; Benavente, Yolanda; Berndt, Sonja I.; Bertrand, Kimberly A.; Birmann, Brenda M.; Boeing, Heiner; Boffetta, Paolo; Bracci, Paige M.; Brennan, Paul; Brooks‐Wilson, Angela; Cerhan, James R.; Chanock, Stephen J.; Clavel, Jacqueline; Conde, Lucía; Cotenbader, Karen H.; Cox, David G.; Cozen, Wendy; Crouch, Simon; Roos, Anneclaire J. De; Sanjosé, Sílvia de; Lollo, Simonetta Di; Diver, W. Ryan; Doğan, Ahmet; Foretová, Lenka; Ghesquières, Hervé; Giles, Graham G.; Glimelius, Bengt; Habermann, Thomas M.; Haı̈oun, Corinne; Hartge, Patricia; Hjalgrim, Henrik; Holford, Theodore R.; Holly, Elizabeth A.; Jackson, Rebecca D.; Kaaks, Rudolph; Kane, Eleanor; Kelly, Rachel S.; Klein, Robert J.; Kraft, Peter; Kricker, Anne; Lan, Qing; Lawrence, Charles E.; Liebow, Mark; Lightfoot, Tracy; Link, Brian K.; Maynadié, Marc; McKay, James; Melbye, Mads; Molina, Thierry Jo; Monnereau, Alain; Morton, Lindsay M.; Nieters, Alexandra; North, Kari E.; Novak, Anne J.; Offit, Kenneth; Purdue, Mark P.; Rais, Marco; Riby, Jacques; Roman, Eve; Rothman, Nathaniel; Salles, Gilles; Severi, Gianluca; Severson, Richard K.; Skibola, Christine F.; Slager, Susan L.; Smith, Alex; Smith, Martyn T.; Southey, Melissa C.; Staines, Anthony; Teras, Lauren R.; Thompson, Carrie A.; Tilly, Hervé; Tinker, Lesley F.; Tjønneland, Anne; Turner, Jennifer; Vajdic, Claire M.; Vermeulen, Roel; Vijai, Joseph; Víneis, Paolo; Virtamo, Jarmo; Wang, Zhaoming; Weinstein, Stephanie J.; Witzig, Thomas E.; Zelenetz, Andrew D.; Zeleniuch‐Jacquotte, Anne; Zhang, Yawei; Zheng, Tongzhang; Zucca, Mariagrazia; Clarke, Ann E.

doi:10.1136/lupus-2016-000187

Cited by 15 publications

(10 citation statements)

References 16 publications

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“…[34] However, in our analyses of genome wide association studies (GWAS), data could not confirm a strong relationship with the lupusrelated TNFAIP3 single nucleotide polymorphism (SNP) rs7749323 specifically for DLBCL; this could be explained by a lack of power due to the sample size. [35] In those GWAS analyses, the rs2205960 SNP, related to TNFSF4, was associated with an odds ratio (OR) per risk allele of 1.07 (95% CI 1.00-1.16). SLE interferon regulatory factor risk allele rs12537284 (chromosome 7q32, IRF5 gene) was associated with an OR of 1.08 (95% CI 0.99-1.18).…”

Section: Polymorphism Of Tnf Alpha-induced Protein 3 (Tnfaip3) and Other Genetic Factorsmentioning

confidence: 99%

Cancer and Systemic Lupus Erythematosus

Ladouceur¹,

Tessier‐Cloutier²,

Clarke³

et al. 2020

Rheumatic Disease Clinics of North America

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Section: Polymorphism Of Tnf Alpha-induced Protein 3 (Tnfaip3) and Other Genetic Factorsmentioning

confidence: 99%

Cancer and Systemic Lupus Erythematosus

Ladouceur¹,

Tessier‐Cloutier²,

Clarke³

et al. 2020

Rheumatic Disease Clinics of North America

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“…Additionally, a GWAS of 3857 DLBCL cases and 7666 controls used previously systemic lupus erythematosus (SLE) associated loci to evaluate the risk of DLBLC, finding HLA risk allele rs1270942. Another study evaluated multiple sclerosis (MS) and rheumatoid arthritis (RA) with DLBCL risk, but not genome-wide significance was reached [ 11 , 19 ]. Moreover, HLA homozygosity was found to be associated with increased DLBCL risk for HLA-B, HLA-C and HLA-DRB1 alleles among Europeans [ 35 ].…”

Section: Gwas In B-cell Nhlmentioning

confidence: 99%

“…A variant is said to be significant at genome-wide level if the p value is ≤5 × 10 −8 , which was set by taking a 0.05 significance level and roughly dividing by the total number of independent blocks of linked genes in Europeans (thought to be 1,000,000) [ 7 , 15 ]. Regarding GWAS within the B-cell NHL context, most studies have focused on genetic variants at chromosome 6p21, specifically human leukocyte antigen (HLA) variants, since that region is critical for innate and adaptive immune responses, but there have been also efforts to find associations with variants outside this chromosome and other etiologies [ 7 , 10 , 11 , 16 , 17 , 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Tracking the Genetic Susceptibility Background of B-Cell Non-Hodgkin’s Lymphomas from Genome-Wide Association Studies

Hernández-Verdin¹,

Labreche²,

Benazra

et al. 2020

IJMS

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B-cell non-Hodgkin’s lymphoma (NHL) risk associations had been mainly attributed to family history of the disease, inflammation, and immune components including human leukocyte antigen (HLA) genetic variations. Nevertheless, a broad range of genome-wide association studies (GWAS) have shed light into the identification of several genetic variants presumptively associated with B-cell NHL etiologies, survival or shared genetic risk with other diseases. The present review aims to overview HLA structure and diversity and summarize the evidence of genetic variations, by GWAS, on five NHL subtypes (diffuse large B-cell lymphoma DLBCL, follicular lymphoma FL, chronic lymphocytic leukemia CLL, marginal zone lymphoma MZL, and primary central nervous system lymphoma PCNSL). Evidence indicates that the HLA zygosity status in B-cell NHL might promote immune escape and that genome-wide significance variants can give biological insight but also potential therapeutic markers such as WEE1 in DLBCL. However, additional studies are needed, especially for non-DLBCL, to replicate the associations found to date.

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“…Using a similar study design, Bernatksy et al [99] examined whether SLE-related SNPs may increase the risk of DLBCL. The frequency of 28 SLE-related SNPs was compared between 3,857 DLBCL cases and 7,666 controls identified from a DLBCL GWAS conducted by the International Lymphoma Epidemiology Consortium (InterLymph).…”

Section: Factors Potentially Mediating Riskmentioning

confidence: 99%

A review on SLE and malignancy

Choi

Flood

Bernatsky

et al. 2017

Best Practice & Research Clinical Rheumatology

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Systemic lupus erythematosus (SLE) is a chronic, systemic autoimmune disease characterized by autoantibody production, complement activation, and immune complex deposition. It predominantly affects young and middle-aged women. While improvements in the diagnosis and treatment of SLE have altered prognosis, morbidity and mortality rates remain higher than the general population. In addition to renal injury, cardiovascular disease, and infection, malignancy is known to be a significant cause of death in this population. There is increasing evidence to suggest that patients with SLE have a slightly higher overall risk of malignancy. The risk of malignancy in SLE is of considerable interest because the immune and genetic pathways underlying the pathogenesis of SLE and the immunosuppressant drugs (ISDs) used in its management may mediate this altered risk. Our current understanding of these and other risk factors and the implications for treating SLE and screening for malignancy is still evolving. This review summarizes the association between SLE and malignancy. The first section discusses the risk of overall and site-specific malignancies in both adult- and pediatric-onset SLE. Next, we evaluate the risk factors and possible mechanisms underlying the link between malignancy and SLE, including the use of ISDs, presence of certain SLE-related autoantibodies, chronic immune dysregulation, environmental factors, and shared genetic susceptibility. Finally, we review guidelines regarding cancer screening and vaccination for human papilloma virus.

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Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma

Cited by 15 publications

References 16 publications

Cancer and Systemic Lupus Erythematosus

Cancer and Systemic Lupus Erythematosus

Tracking the Genetic Susceptibility Background of B-Cell Non-Hodgkin’s Lymphomas from Genome-Wide Association Studies

A review on SLE and malignancy

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