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Nieters A.;Conde L.;Slager S.;Brooks-Wilson A.;Morton L.;Skibola D.;Novak A.;Riby J.;Ansell S.;Halperin E.;Shanafelt T.;Agana L.;Wang A.;De Roos A.;Severson R.;Cozen W.;Spinelli J.;Butterbach K.;Becker N.;De Sanjose S.;Benavente Y.;Cocco P.;Staines A.;Maynadié M.;Foretova L.;Boffetta P.;Brennan P.;Lan Q.;Zhang Y.;Zheng T.;Purdue M.;Armstrong B.;Kricker A.;Vajdic C.;Grulich A.;Smith M.;Bracci P.;Chanock S.;Hartge P.;Cerhan J.;Wang S.;Rothman N.;Skibola C.
PRRC2A and BCL2L11 gene variants influence risk of non-Hodgkin lymphoma: Results from the InterLymph consortium
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Many 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.Ameta-analysis was performed on data from 5633 B-cell NHL cases and 7034 controls from 8 Inter-Lymph 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.
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