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@ARTICLE{Aglago:168193,
      author       = {E. K. Aglago and C. G. Schalkwijk and H. Freisling and V.
                      Fedirko and D. J. Hughes and L. Jiao and C. C. Dahm and A.
                      Olsen and A. Tjønneland and V. Katzke$^*$ and T.
                      Johnson$^*$ and M. B. Schulze and K. Aleksandrova and G.
                      Masala and S. Sieri and V. Simeon and R. Tumino and A.
                      Macciotta and B. Bueno-de-Mesquita and G. Skeie and I. T.
                      Gram and T. Sandanger and P. Jakszyn and M.-J. Sánchez and
                      P. Amiano and S. M. Colorado-Yohar and A. B. Gurrea and A.
                      Perez-Cornago and A.-L. Mayén and E. Weiderpass and M. J.
                      Gunter and A. K. Heath and M. Jenab},
      title        = {{P}lasma concentrations of advanced glycation end-products
                      and colorectal cancer risk in the {EPIC} study.},
      journal      = {Carcinogenesis},
      volume       = {42},
      number       = {5},
      issn         = {1460-2180},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2021-00733},
      pages        = {705-713},
      year         = {2021},
      note         = {2021 May 28;42(5):705-713},
      abstract     = {Advanced glycation end-products (AGEs) are a heterogeneous
                      group of compounds formed by the non-enzymatic reaction
                      between amino-acids and reducing sugars, or dicarbonyls as
                      intermediate compounds. Experimental studies suggest that
                      AGEs may promote colorectal cancer, but prospective
                      epidemiologic studies are inconclusive. We conducted a
                      case-control study nested within a large European cohort.
                      Plasma concentrations of three protein-bound AGEs: N
                      ε-(carboxy-methyl)lysine (CML), N ε-(carboxy-ethyl)lysine
                      (CEL) and N
                      δ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1)
                      were measured by ultra-performance liquid chromatography
                      tandem mass-spectrometry in baseline samples collected from
                      1,378 incident primary colorectal cancer cases and 1,378
                      matched controls. Multivariable-adjusted odds ratios (ORs)
                      and $95\%$ confidence intervals (CIs) were computed using
                      conditional logistic regression for colorectal cancer risk
                      associated with CML, CEL, MG-H1, total AGEs, and [CEL+MG-H1:
                      CML] and [CEL:MG-H1] ratios. Inverse colorectal cancer risk
                      associations were observed for CML (OR comparing highest to
                      lowest quintile, ORQ5vs.Q1=0.40, $95\%CI:0.27-0.59),$ MG-H1
                      (ORQ5vs.Q1=0.73, $95\%CI:0.53$ - 1.00) and total AGEs (OR
                      Q5vs.Q1=0.52, $95\%CI:0.37$ - 0.73) whereas no association
                      was observed for CEL. A higher [CEL+MG-H1: CML] ratio was
                      associated with colorectal cancer risk (ORQ5vs.Q1=1.91,
                      $95\%CI:1.31-2.79).$ The associations observed did not
                      differ by sex, or by tumour anatomical subsite. Although
                      individual AGEs concentrations appear to be inversely
                      associated with colorectal cancer risk, a higher ratio of
                      methylglyoxal-derived AGEs versus those derived from glyoxal
                      (calculated by [CEL+MG-H1: CML] ratio) showed a strong
                      positive risk association. Further insight on the metabolism
                      of AGEs and their dicarbonyls precursors, and their roles in
                      colorectal cancer development is needed.},
      keywords     = {Advanced glycation end-product (Other) / colorectal cancer
                      (Other) / glycotoxin (Other)},
      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:33780524},
      doi          = {10.1093/carcin/bgab026},
      url          = {https://inrepo02.dkfz.de/record/168193},
}