Citations 3
Genetically determined body mass index is associated with diffuse large B‐cell lymphoma in polygenic and Mendelian randomization analyses
Moore, Amy , Teras, Lauren R. , Machiela, Mitchell J. , Arias, Joshua , Monnereau, Alain , Wang, Zhaoming , Vermeulen, Roel , Smedby, Karin E. , Spinelli, John J., Nieters, Alexandra , Bracci, Paige M. , Camp, Nicola J. , Hjalgrim, Henrik, Adami, Hans‐Olov , Albanes, Demetrius, Becker, Nikolaus, Benavente, Yolanda , Clavel, Jacqueline , Curtin, Karen , Ghesquières, Hervé, Glimelius, Bengt, Lan, Qing , Liebow, Mark , McKay, James , Offit, Kenneth, Padoan, Marina, Patel, Alpa V. , Ríboli, Elio , Severson, Richard K., Tinker, Lesley F. , Weinstein, Stephanie J. , Zheng, Tongzhang, Chanock, Stephen J., Rothman, Nathaniel , Berndt, Sonja I. , Teras, Lauren R , Wang, Zhaoming , Vajdic, Claire M , De Vivo, Immaculata , Boffetta, Paolo , Brooks-Wilson, Angela R , Canzian, Federico , Southey, Melissa C , Cerhan, James R , Berndt, Sonja I , Clavel, Jacqueline , Machiela, Mitchell J , Riboli, Elio , Kane, Eleanor , Panagiotou, Orestis A. , Doo, Nicole Wong , Slager, Susan L. , Vajdic, Claire M. , Vijai, Joseph , Giles, Graham G. , Link, Brian K. , Arslan, Alan A. , Salles, Gilles , Cozen, Wendy , Vivo, Immaculata De , Albanes, Demetrius , Bisanzi, Simonetta , Brennan, Paul E. , Brooks‐Wilson, Angela , Canzian, Federico , Conde, Lucía , Cox, David G. , Foretová, Lenka , Glimelius, Bengt , Habermann, Thomas M. , Hofmann, Jonathan N. , Lan, Qing , Lincoln, Anne , Maynadié, Marc , Melbye, Mads , Miligi, Lucia , Milne, Roger L. , Molina, Thierry Jo , Morton, Lindsay M. , North, Kari E. , Offit, Kenneth, Piro, Sara , Purdue, Mark P. , Ravichandran, Vignesh , Southey, Melissa C. , Staines, Anthony , Travis, Ruth C. , Wang, Sophia , Weiderpass, Elisabete , Rothman, Nathaniel , Birmann, Brenda M. , Cerhan, James R.
International Journal of Cancer | September 5, 2025 | Volume: 158 | Issue: 1 | Pages: 45-59
Abstract Obesity has been associated with non‐Hodgkin lymphoma (NHL), but the evidence is inconclusive. We examined the association between genetically determined adiposity and four common NHL subtypes: diffuse large B‐cell lymphoma (DLBCL), follicular lymphoma, chronic lymphocytic leukemia, and marginal zone lymphoma, using eight genome‐wide association studies of European ancestry ( N = 10,629 cases, 9505 controls) and constructing polygenic scores for body mass index (BMI), waist‐to‐hip ratio (WHR), and waist‐to‐hip ratio adjusted for BMI (WHRadjBMI). Higher genetically determined BMI was associated with an increased risk of DLBCL [odds ratio (OR) per standard deviation (SD) = 1.18, 95% confidence interval (95% CI): 1.05–1.33, p = .005]. This finding was consistent with Mendelian randomization analyses, which demonstrated a similar increased risk of DLBCL with higher genetically determined BMI (OR per SD = 1.12, 95% CI: 1.02–1.23, p = .03). No significant associations were observed with other NHL subtypes. Our study demonstrates a positive link between a genetically determined BMI and an increased risk of DLBCL, providing additional support for increased adiposity as a risk factor for DLBCL.
Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypes
Din, Lennox, Kosaraju, Nikitha , Smedby, Karin E. , Berndt, Sonja I. , Skibola, Christine F., Nieters, Alexandra, Wang, Sophia , McKay, James , Cocco, Pierluigi , Foretová, Lenka , Staines, Anthony , Mack, Thomas M. , Sanjosé, Sílvia de , Vyse, Timothy J. , Padyukov, Leonid , Monnereau, Alain , Arslan, Alan A. , Moore, Amy , Brooks‐Wilson, Angela , Novak, Anne J. , Glimelius, Bengt , Birmann, Brenda M. , Link, Brian K. , Stewart, Carolyn, Vajdic, Claire M. , Magnani, Corrado , Conti, David V. , Cox, David G. , Casabonne, Delphine, Kane, Eleanor , Roman, Eve , Salles, Gilles , Adami, Hans‐Olov , Ghesquières, Hervé , Vivo, Immaculata De , Clavel, Jacqueline , Spinelli, John J., Curtin, Karen , Costenbader, Karen H. , Onel, Kenan , Offit, Kenneth , Morton, Lindsay M. , Conde, Lucía , Miligi, Lucia , Melbye, Mads , Liebow, Mark , Purdue, Mark P. , Glenn, Martha, Din, M. Azhar Ud, Rothman, Nathaniel , Camp, Nicola J. , Doo, Nicole Wong , Becker, Nikolaus, Pradhan, Nisha , Bracci, Paige M. , Vineis, Paolo , Brennan, Paul , Kraft, Peter , Lan, Qing , Severson, Richard K., Vermeulen, Roel , Kaaks, Rudolph, Travis, Ruth C. , Weinstein, Stephanie J. , Ansell, Stephen M. , Zheng, Tongzhang, Benavente, Yolanda , Taub, Zachary, Madireddy, Lohith, Gourraud, Pierre‐Antoine , Oksenberg, Jorge R. , Hjalgrim, Henrik , Khankhanian, Pouya , Cerhan, James R , Khankhanian, Pouya , Link, Brian K , Cocco, Pierluigi , Brooks-Wilson, Angela R , Vajdic, Claire M , Kane, Eleanor , Arslan, Alan A , Travis, Ruth C , De Vivo, Immaculata , Kraft, Peter , Morton, Lindsay M , Padyukov, Leonid , Salles, Gilles A , Wang, Sophia S , Birmann, Brenda M , Roman, Eve , Clavel, Jacqueline , Conti, David V , Doo, Nicole Wong , Sheikh, Mohammad, Bernatsky, Sasha , Maynadié, Marc , Haïoun, Corinne , Casabonne, Delphine , Albanes, Demetrius , Muzi, Giacomo , Giles, Graham G. , Cerhan, James R. , Hofmann, Jonathan N. , Vijai, Joseph , Teras, Lauren R. , Ennas, Maria Grazia , Southey, Melissa C. , Boffetta, Paolo , Milne, Roger L. , Chanock, Stephen Jacob , Slager, Susan L. , Zhang, Yawei , Cozen, Wendy
Genetic Epidemiology | August 13, 2019 | Volume: 43 | Issue: 7 | Pages: 844-863
AbstractEpidemiologic 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.
Association of polygenic risk score with the risk of chronic lymphocytic leukemia and monoclonal B-cell lymphocytosis
Kleinstern, Geffen , Camp, Nicola J. , Goldin, Lynn R. , Vachon, Celine M. , Vajdic, Claire M. , Sanjosé, Sílvia de, Weinberg, J. Brice , Benavente, Yolanda , Casabonne, Delphine, Liebow, Mark , Nieters, Alexandra, Hjalgrim, Henrik , Melbye, Mads , Glimelius, Bengt , Adami, Hans‐Olov , Brennan, Paul , McKay, James , Cocco, Pier Luigi, Call, Timothy G. , Hanson, Curtis A. , Robinson, Dennis P. , Chaffee, Kari G. , Brooks‐Wilson, Angela , Monnereau, Alain, Clavel, Jacqueline , Glenn, Martha, Curtin, Karen , Conde, Lucía , Bracci, Paige M. , Morton, Lindsay M. , Severson, Richard K., Chanock, Stephen J., Spinelli, John J., Johnston, James B. , Rothman, Nathaniel , Skibola, Christine F., Leis, José F., Smedby, Karin E. , Berndt, Sonja I. , Caporaso, Neil E., Rabe, Kari G. , Cocco, Pierluigi , Monnereau, Alain , Norman, Aaron D. , Hanson, Curtis, Robinson, Dennis, Cocco, Pierluigi , Brooks-Wilson, Angela R , Vajdic, Claire M , Morton, Lindsay M , Clavel, Jacqueline , Vachon, Celine M. , Casabonne, Delphine , Boffetta, Paolo , Maynadié, Marc , Shanafelt, Tait D. , Cozen, Wendy , Rothman, Nathaniel , Kay, Neil E. , Cerhan, James R. , Slager, Susan L.
Blood | April 19, 2018 | Volume: 131 | Issue: 23 | Pages: 2541-2551
Key Points PRS, based on the known CLL loci, predicts CLL risk with high discrimination. This PRS predicts risk of monoclonal B-cell lymphocytosis, a precursor to CLL and a condition that has clinical impact beyond risk for CLL.