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@ARTICLE{SnchezMaldonado:157166,
      author       = {J. M. Sánchez-Maldonado and D. Campa and J. Springer and
                      J. Badiola and Y. Niazi$^*$ and A. Moñiz-Díez and F.
                      Hernández-Mohedo and P. González-Sierra and R. Ter Horst
                      and A. Macauda$^*$ and S. Brezina and C. Cunha and M.
                      Lackner and M. A. López-Nevot and L. Fianchi and L. Pagano
                      and E. López-Fernández and L. Potenza and M. Luppi and L.
                      Moratalla and J. J. Rodríguez-Sevilla and J. E. Fonseca and
                      M. Tormo and C. Solano and E. Clavero and A. Romero and Y.
                      Li and C. Lass-Flörl and H. Einsele and L. Vazquez and J.
                      Loeffler and K. Hemminki$^*$ and A. Carvalho and M. G. Netea
                      and A. Gsur and C. Dumontet and F. Canzian$^*$ and A.
                      Försti$^*$ and M. Jurado and J. Sainz},
      title        = {{H}ost immune genetic variations influence the risk of
                      developing acute myeloid leukaemia: results from the
                      {N}u{CLEAR} consortium.},
      journal      = {Blood cancer journal},
      volume       = {10},
      number       = {7},
      issn         = {2044-5385},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2020-01446},
      pages        = {75},
      year         = {2020},
      abstract     = {The 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.},
      cin          = {C050 / B062 / C055 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)C050-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)C055-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32678078},
      doi          = {10.1038/s41408-020-00341-y},
      url          = {https://inrepo02.dkfz.de/record/157166},
}