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Riby, Jacques

Mayo Clinic

University of Alabama at Birmingham

Citations 3

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

Lupus Science & Medicine | November 13, 2017 | Volume: 4 | Issue: 1 | Pages: e000187

10.1136/lupus-2016-000187 Get It

Objective Determinants of the increased risk of diffuse large B-cell lymphoma (DLBCL) in SLE are unclear. Using data from a recent lymphoma genome-wide association study (GWAS), we assessed whether certain lupus-related single nucleotide polymorphisms (SNPs) were also associated with DLBCL. Methods GWAS data on European Caucasians from the International Lymphoma Epidemiology Consortium (InterLymph) provided a total of 3857 DLBCL cases and 7666 general-population controls. Data were pooled in a random-effects meta-analysis. Results Among the 28 SLE-related SNPs investigated, the two most convincingly associated with risk of DLBCL included the CD40 SLE risk allele rs4810485 on chromosome 20q13 (OR per risk allele=1.09, 95% CI 1.02 to 1.16, p=0.0134), and the HLA SLE risk allele rs1270942 on chromosome 6p21.33 (OR per risk allele=1.17, 95% CI 1.01 to 1.36, p=0.0362). Of additional possible interest were rs2205960 and rs12537284. The rs2205960 SNP, related to a cytokine of the tumour necrosis factor superfamily TNFSF4, was associated with an OR per risk allele of 1.07, 95% CI 1.00 to 1.16, p=0.0549. The OR for the rs12537284 (chromosome 7q32, IRF5 gene) risk allele was 1.08, 95% CI 0.99 to 1.18, p=0.0765. Conclusions These data suggest several plausible genetic links between DLBCL and SLE.
PRRC2A and BCL2L11 gene variants influence risk of non-Hodgkin lymphoma: results from the InterLymph consortium
Nieters, Alexandra, Conde, Lucía , Morton, Lindsay M. , Skibola, Danica R., Novak, Anne J. , Riby, Jacques, Ansell, Stephen M. , Halperin, Eran , Agana, Luz, Wang, Alice H., Roos, Anneclaire J. De , Severson, Richard K., Spinelli, John, Butterbach, Katja, Becker, Nikolaus, Sanjosé, Sílvia de , Benavente, Yolanda , Cocco, Pierluigi , Staines, Anthony , Foretová, Lenka , Brennan, Paul , Lan, Qing , Zheng, Tongzhang, Purdue, Mark P. , Armstrong, Bruce K. , Kricker, Anne , Vajdic, Claire M. , Grulich, Andrew E. , Smith, Martyn T. , Bracci, Paige M. , Hartge, Patricia, Cerhan, James R. , Wang, Sophia , Rothman, Nathaniel , Skibola, Christine F., Slager, Susan L. , Brooks‐Wilson, Angela , Shanafelt, Tait D. , Cozen, Wendy , Maynadié, Marc , Boffetta, Paolo , Zhang, Yawei , Chanock, Stephen Jacob , Cerhan, James R , Cocco, Pierluigi , Vajdic, Claire M , Morton, Lindsay M , De Roos, Anneclaire J , Wang, Sophia S

Blood | October 10, 2012 | Volume: 120 | Issue: 23 | Pages: 4645-4648

10.1182/blood-2012-05-427989 Get It

AbstractMany common genetic variants have been associated with non-Hodgkin lymphoma (NHL), but individual study results are often conflicting. To confirm the role of putative risk alleles in B-cell NHL etiology, we performed a validation genotyping study of 67 candidate single nucleotide polymorphisms within InterLymph, a large international consortium of NHL case-control studies. A meta-analysis was performed on data from 5633 B-cell NHL cases and 7034 controls from 8 InterLymph studies. rs3789068 in the proapoptotic BCL2L11 gene was associated with an increased risk for B-cell NHL (odds ratio = 1.21, P random = 2.21 × 10−11), with similar risk estimates for common B-cell subtypes. PRRC2A rs3132453 in the HLA complex class III region conferred a reduced risk of B-cell NHL (odds ratio = 0.68, P random = 1.07 × 10−9) and was likewise evident for common B-cell subtypes. These results are consistent with the known biology of NHL and provide insights into shared pathogenic components, including apoptosis and immune regulation, for the major B-cell lymphoma subtypes.
Common variation at 6p21.31 (BAK1) influences the risk of chronic lymphocytic leukemia
Skibola, Christine F., Bernardo, Maria Chiara Di, Conde, Lucía , Broderick, Peter , McDonnell, Shannon K. , Goldin, Lynn R. , Croft, Naomi, Holroyd, Amy, Harris, Shelley , Riby, Jacques, Serie, Daniel, Call, Timothy G. , Bracci, Paige M. , Halperin, Eran , Lanasa, Mark C., Cunningham, Julie M. , Leis, José F., Morrison, Vicki A., Spector, Logan G. , Vachon, Celine M. , Strom, Sara S., Camp, Nicola J. , Weinberg, J. Brice , Matutes, Estella , Caporaso, Neil E., Wade, Rachel , Dyer, Martin J.S. , Dearden, Claire , Cerhan, James R. , Catovsky, Daniel , Houlston, Richard S. , Slager, Susan L. , Kay, Neil E. , Vachon, Celine M. , Shanafelt, Tait D. , Cerhan, James R , Houlston, Richard S , McDonnell, Shannon K

Blood | June 15, 2012 | Volume: 120 | Issue: 4 | Pages: 843-846

10.1182/blood-2012-03-413591 Get It

Abstract We performed a meta-analysis of 3 genome-wide association studies to identify additional common variants influencing chronic lymphocytic leukemia (CLL) risk. The discovery phase was composed of genome-wide association study data from 1121 cases and 3745 controls. Replication analysis was performed in 861 cases and 2033 controls. We identified a novel CLL risk locus at 6p21.33 (rs210142; intronic to the BAK1 gene, BCL2 antagonist killer 1; P = 9.47 × 10−16). A strong relationship between risk genotype and reduced BAK1 expression was shown in lymphoblastoid cell lines. This finding provides additional support for polygenic inheritance to CLL and provides further insight into the biologic basis of disease development.