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000157166 1001_ $$aSánchez-Maldonado, J. M.$$b0
000157166 245__ $$aHost immune genetic variations influence the risk of developing acute myeloid leukaemia: results from the NuCLEAR consortium.
000157166 260__ $$aLondon [u.a.]$$bNature Publishing Group$$c2020
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000157166 520__ $$aThe purpose of this study was to conduct a two-stage case control association study including 654 acute myeloid leukaemia (AML) patients and 3477 controls ascertained through the NuCLEAR consortium to evaluate the effect of 27 immune-related single nucleotide polymorphisms (SNPs) on AML risk. In a pooled analysis of cohort studies, we found that carriers of the IL13rs1295686A/A genotype had an increased risk of AML (PCorr = 0.0144) whereas carriers of the VEGFArs25648T allele had a decreased risk of developing the disease (PCorr = 0.00086). In addition, we found an association of the IL8rs2227307 SNP with a decreased risk of developing AML that remained marginally significant after multiple testing (PCorr = 0.072). Functional experiments suggested that the effect of the IL13rs1295686 SNP on AML risk might be explained by its role in regulating IL1Ra secretion that modulates AML blast proliferation. Likewise, the protective effect of the IL8rs2227307 SNP might be mediated by TLR2-mediated immune responses that affect AML blast viability, proliferation and chemorresistance. Despite the potential interest of these results, additional functional studies are still warranted to unravel the mechanisms by which these variants modulate the risk of AML. These findings suggested that IL13, VEGFA and IL8 SNPs play a role in modulating AML risk.
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000157166 7001_ $$aCampa, D.$$b1
000157166 7001_ $$aSpringer, J.$$b2
000157166 7001_ $$00000-0003-0660-9186$$aBadiola, J.$$b3
000157166 7001_ $$0P:(DE-He78)0681b959321f574e7ad1869cc3011346$$aNiazi, Y.$$b4$$udkfz
000157166 7001_ $$aMoñiz-Díez, A.$$b5
000157166 7001_ $$aHernández-Mohedo, F.$$b6
000157166 7001_ $$00000-0002-6492-1728$$aGonzález-Sierra, P.$$b7
000157166 7001_ $$aTer Horst, R.$$b8
000157166 7001_ $$0P:(DE-He78)b791a47b92809f7c54501331f72e0243$$aMacauda, A.$$b9$$udkfz
000157166 7001_ $$00000-0001-5238-6900$$aBrezina, S.$$b10
000157166 7001_ $$aCunha, C.$$b11
000157166 7001_ $$aLackner, M.$$b12
000157166 7001_ $$aLópez-Nevot, M. A.$$b13
000157166 7001_ $$aFianchi, L.$$b14
000157166 7001_ $$00000-0001-8287-928X$$aPagano, L.$$b15
000157166 7001_ $$aLópez-Fernández, E.$$b16
000157166 7001_ $$aPotenza, L.$$b17
000157166 7001_ $$aLuppi, M.$$b18
000157166 7001_ $$aMoratalla, L.$$b19
000157166 7001_ $$aRodríguez-Sevilla, J. J.$$b20
000157166 7001_ $$aFonseca, J. E.$$b21
000157166 7001_ $$aTormo, M.$$b22
000157166 7001_ $$aSolano, C.$$b23
000157166 7001_ $$aClavero, E.$$b24
000157166 7001_ $$aRomero, A.$$b25
000157166 7001_ $$aLi, Y.$$b26
000157166 7001_ $$aLass-Flörl, C.$$b27
000157166 7001_ $$aEinsele, H.$$b28
000157166 7001_ $$aVazquez, L.$$b29
000157166 7001_ $$aLoeffler, J.$$b30
000157166 7001_ $$0P:(DE-He78)19b0ec1cea271419d9fa8680e6ed6865$$aHemminki, K.$$b31$$udkfz
000157166 7001_ $$00000-0001-8935-8030$$aCarvalho, A.$$b32
000157166 7001_ $$aNetea, M. G.$$b33
000157166 7001_ $$00000-0002-9795-1528$$aGsur, A.$$b34
000157166 7001_ $$aDumontet, C.$$b35
000157166 7001_ $$0P:(DE-He78)5323704270b6393dcea70186ffd86bca$$aCanzian, F.$$b36$$udkfz
000157166 7001_ $$0P:(DE-He78)f26164c08f2f14abcf31e52e13ee3696$$aFörsti, A.$$b37$$udkfz
000157166 7001_ $$aJurado, M.$$b38
000157166 7001_ $$00000-0002-9355-2423$$aSainz, J.$$b39
000157166 773__ $$0PERI:(DE-600)2600560-8$$a10.1038/s41408-020-00341-y$$gVol. 10, no. 7, p. 75$$n7$$p75$$tBlood cancer journal$$v10$$x2044-5385$$y2020
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