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@ARTICLE{Dimou:277118,
      author       = {N. Dimou and A. E. Kim and O. Flanagan and N. Murphy and V.
                      Diez-Obrero and A. Shcherbina and E. K. Aglago and E. Bouras
                      and P. T. Campbell and G. Casey and S. Gallinger and S. B.
                      Gruber and M. A. Jenkins and Y. Lin and V. Moreno and E.
                      Ruiz-Narvaez and M. C. Stern and Y. Tian$^*$ and K. K.
                      Tsilidis and V. Arndt$^*$ and E. L. Barry and J. W. Baurley
                      and S. I. Berndt and S. Bézieau and S. A. Bien and D. T.
                      Bishop and H. Brenner$^*$ and A. Budiarto and R.
                      Carreras-Torres and T. W. Cenggoro and A. T. Chan and J.
                      Chang-Claude$^*$ and S. J. Chanock and X. Chen$^*$ and D. V.
                      Conti and C. H. Dampier and M. Devall and D. A. Drew and J.
                      C. Figueiredo and G. G. Giles and A. Gsur and T. A. Harrison
                      and A. Hidaka and M. Hoffmeister$^*$ and J. R. Huyghe and K.
                      Jordahl and E. Kawaguchi and T. O. Keku and S. C. Larsson
                      and L. Le Marchand and J. P. Lewinger and L. Li and B.
                      Mahesworo and J. Morrison and P. A. Newcomb and C. C. Newton
                      and M. Obon-Santacana and J. Ose and R. K. Pai and J. R.
                      Palmer and N. Papadimitriou and B. Pardamean and A. R.
                      Peoples and P. D. P. Pharoah and E. A. Platz and J. D.
                      Potter and G. Rennert and P. C. Scacheri and R. E. Schoen
                      and Y.-R. Su and C. M. Tangen and S. N. Thibodeau and D. C.
                      Thomas and C. M. Ulrich and C. Y. Um and F. J. B. van
                      Duijnhoven and K. Visvanathan and P. Vodicka and L.
                      Vodickova and E. White and A. Wolk and M. O. Woods and C. Qu
                      and A. Kundaje and L. Hsu and W. J. Gauderman and M. J.
                      Gunter and U. Peters},
      title        = {{P}robing the diabetes and colorectal cancer relationship
                      using gene - environment interaction analyses.},
      journal      = {British journal of cancer},
      volume       = {129},
      number       = {3},
      issn         = {0007-0920},
      address      = {Edinburgh},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2023-01283},
      pages        = {511-520},
      year         = {2023},
      note         = {2023 Aug;129(3):511-520},
      abstract     = {Diabetes is an established risk factor for colorectal
                      cancer. However, the mechanisms underlying this relationship
                      still require investigation and it is not known if the
                      association is modified by genetic variants. To address
                      these questions, we undertook a genome-wide gene-environment
                      interaction analysis.We used data from 3 genetic consortia
                      (CCFR, CORECT, GECCO; 31,318 colorectal cancer cases/41,499
                      controls) and undertook genome-wide gene-environment
                      interaction analyses with colorectal cancer risk, including
                      interaction tests of genetics(G)xdiabetes (1-degree of
                      freedom; d.f.) and joint testing of Gxdiabetes, G-colorectal
                      cancer association (2-d.f. joint test) and G-diabetes
                      correlation (3-d.f. joint test).Based on the joint tests, we
                      found that the association of diabetes with colorectal
                      cancer risk is modified by loci on chromosomes 8q24.11
                      (rs3802177, SLC30A8 - ORAA: 1.62, $95\%$ CI: 1.34-1.96;
                      ORAG: 1.41, $95\%$ CI: 1.30-1.54; ORGG: 1.22, $95\%$ CI:
                      1.13-1.31; p-value3-d.f.: 5.46 × 10-11) and 13q14.13
                      (rs9526201, LRCH1 - ORGG: 2.11, $95\%$ CI: 1.56-2.83; ORGA:
                      1.52, $95\%$ CI: 1.38-1.68; ORAA: 1.13, $95\%$ CI:
                      1.06-1.21; p-value2-d.f.: 7.84 × 10-09).These results
                      suggest that variation in genes related to insulin signaling
                      (SLC30A8) and immune function (LRCH1) may modify the
                      association of diabetes with colorectal cancer risk and
                      provide novel insights into the biology underlying the
                      diabetes and colorectal cancer relationship.},
      cin          = {C020 / C070 / C120 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331 / 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:37365285},
      doi          = {10.1038/s41416-023-02312-z},
      url          = {https://inrepo02.dkfz.de/record/277118},
}