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@ARTICLE{Aglago:164096,
      author       = {E. K. Aglago and S. Rinaldi and H. Freisling and L. Jiao
                      and D. J. Hughes and V. Fedirko and C. G. Schalkwijk and E.
                      Weiderpass and C. C. Dahm and K. Overvad and A. K. Eriksen
                      and C. Kyrø and M.-C. Boutron-Ruault and J. A. Rothwell and
                      G. Severi and V. Katzke$^*$ and T. Kühn$^*$ and M. B.
                      Schulze and K. Aleksandrova and G. Masala and V. Krogh and
                      S. Panico and R. Tumino and A. Naccarati and B.
                      Bueno-de-Mesquita and C. H. van Gils and T. M. Sandanger and
                      I. T. Gram and G. Skeie and J. R. Quirós and P. Jakszyn and
                      M.-J. Sánchez and P. Amiano and J. M. Huerta and E. Ardanaz
                      and I. Johansson and S. Harlid and A. Perez-Cornago and
                      A.-L. Mayén and R. Cordova and M. J. Gunter and P. Vineis
                      and A. J. Cross and E. Riboli and M. Jenab},
      title        = {{S}oluble {R}eceptor for {A}dvanced {G}lycation
                      {E}nd-products (s{RAGE}) and colorectal cancer risk: a
                      case-control study nested within a {E}uropean prospective
                      cohort.},
      journal      = {Cancer epidemiology, biomarkers $\&$ prevention},
      volume       = {30},
      number       = {1},
      issn         = {1538-7755},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2020-02242},
      pages        = {182-192},
      year         = {2021},
      note         = {2021 Jan;30(1):182-192},
      abstract     = {Overexpression of the Receptor for Advanced Glycation
                      End-product (RAGE) has been associated with chronic
                      inflammation, which in turn has been associated with
                      increased colorectal cancer (CRC) risk. Soluble RAGE (sRAGE)
                      competes with RAGE to bind its ligands, thus potentially
                      preventing RAGE-induced inflammation.To investigate whether
                      sRAGE and related genetic variants are associated with CRC
                      risk, we conducted a nested case-control study in the
                      European Prospective Investigation into Cancer and Nutrition
                      (EPIC). Plasma sRAGE concentrations were measured by ELISA
                      in 1,361 CRC matched case-control sets. Twenty-four single
                      nucleotide polymorphisms (SNPs) encoded in the genes
                      associated with sRAGE concentrations were available for
                      1,985 CRC cases and 2,220 controls. Multivariable-adjusted
                      odds ratios (ORs) and $95\%$ confidence intervals (CIs) were
                      computed using conditional and unconditional logistic
                      regression for CRC risk and circulating sRAGE and SNPs,
                      respectively.Higher sRAGE concentrations were inversely
                      associated with CRC (ORQ5vs.Q1=0.77, $95\%CI=0.59-1.00).$
                      Sex-specific analyses revealed that the observed inverse
                      risk association was restricted to men (ORQ5vs.Q1=0.63,
                      $95\%CI=0.42-0.94)$ whereas no association was observed in
                      women (ORQ5vs.Q1=1.00, $95\%CI=0.68-1.48,$ Pheterogeneity
                      for sex=0.006). Participants carrying minor allele of
                      rs653765 (promoter region of ADAM10) had lower CRC risk (C
                      vs. T, OR=0.90; $95\%CI=0.82-0.99).Pre-diagnostic$ sRAGE
                      concentrations were inversely associated with CRC risk in
                      men but not in women. A SNP located within ADAM10 gene
                      pertaining to RAGE shedding, was associated with CRC
                      risk.Further studies are needed to confirm our observed sex
                      difference in the association and better explore the
                      potential involvement of genetic variants of sRAGE in CRC
                      development.},
      cin          = {C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33082206},
      doi          = {10.1158/1055-9965.EPI-20-0855},
      url          = {https://inrepo02.dkfz.de/record/164096},
}