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@ARTICLE{Aglago:291763,
      author       = {E. K. Aglago and C. Qu and S. Harlid and A. I. Phipps and
                      R. S. Steinfelder and S. Ogino and C. E. Thomas and L. Hsu
                      and A. E. Toland and H. Brenner$^*$ and S. I. Berndt and D.
                      D. Buchanan and P. T. Campbell and Y. Cao and A. T. Chan and
                      D. A. Drew and J. C. Figueiredo and A. J. French and S.
                      Gallinger and P. Georgeson and M. Giannakis and E. L. Goode
                      and S. B. Gruber and M. J. Gunter and T. A. Harrison and M.
                      Hoffmeister$^*$ and W.-Y. Huang and M. A. Hullar and J. R.
                      Huyghe and M. A. Jenkins and B. M. Lynch and V. Moreno and
                      N. Murphy and C. C. Newton and J. A. Nowak and M.
                      Obón-Santacana and W. Sun and T. Ugai and C. Y. Um and S.
                      H. Zaidi and K. K. Tsilidis and B. van Guelpen and U.
                      Peters},
      title        = {{F}olate intake and colorectal cancer risk according to
                      genetic subtypes defined by targeted tumor sequencing.},
      journal      = {The American journal of clinical nutrition},
      volume       = {120},
      number       = {3},
      issn         = {0095-9871},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-01499},
      pages        = {664-673},
      year         = {2024},
      note         = {2024 Sep;120(3):664-673},
      abstract     = {Folate is involved in multiple genetic, epigenetic, and
                      metabolic processes, and inadequate folate intake has been
                      associated with an increased risk of cancer.We examined
                      whether folate intake is differentially associated with
                      colorectal cancer (CRC) risk according to somatic mutations
                      in genes linked to CRC using targeted
                      sequencing.Participants within two large CRC consortia with
                      available information on dietary folate, supplemental folic
                      acid, and total folate intake were included. Colorectal
                      tumor samples from cases were sequenced for the presence of
                      non-silent mutations in 105 genes and 6 signaling pathways
                      (IGF2/PI3K, MMR, RTK/RAS, TGF-β, WNT, TP53/ATM).
                      Multinomial logistic regression models were run comparing
                      mutated/non-mutated CRC cases to controls to compute
                      multivariable-adjusted odds ratios (ORs) with $95\%$
                      confidence intervals (CI). Heterogeneity of associations of
                      mutated versus non-mutated CRC cases was tested in case-only
                      analyses using logistic regression. Analyses were performed
                      separately in hypermutated and non-hypermutated tumors, as
                      they exhibit different clinical behaviors.We included 4,339
                      CRC cases (702 hypermutated tumors, $16.2\%)$ and 11,767
                      controls. Total folate intake was inversely associated with
                      CRC risk (OR=0.93, $95\%CI=0.90-0.96).$ Among hypermutated
                      tumors, 12 genes (AXIN2, B2M, BCOR, CHD1, DOCK3, FBLN2,
                      MAP3K21, POLD1, RYR1, TET2, UTP20, ZNF521) showed nominal
                      statistical significance (P<0.05) for heterogeneity by
                      mutation status, but none remained significant after
                      multiple testing correction. Among these genetic subtypes,
                      the associations between folate variables and CRC were
                      mostly inverse or towards the null, except for tumors
                      mutated for DOCK3 (supplemental folic acid), CHD1 (total
                      folate), and ZNF521 (dietary folate) that showed positive
                      associations. We did not observe differential associations
                      in analyses among non-hypermutated tumors, or according to
                      the signaling pathways.Folate intake was not differentially
                      associated with CRC risk according to mutations in the genes
                      explored. The nominally significant differential mutation
                      effects observed in a few genes warrants further
                      investigation.},
      keywords     = {colorectal cancer (Other) / folate (Other) / folic acid
                      (Other) / molecular subtypes (Other) / somatic mutations
                      (Other) / tumor (Other)},
      cin          = {C070 / C120 / HD01},
      ddc          = {570},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39025327},
      doi          = {10.1016/j.ajcnut.2024.07.012},
      url          = {https://inrepo02.dkfz.de/record/291763},
}