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@ARTICLE{Tian:180090,
      author       = {Y. Tian$^*$ and A. E. Kim and S. A. Bien and Y. Lin and C.
                      Qu and T. Harrison and R. Carreras-Torres and V.
                      Díez-Obrero and N. Dimou and D. A. Drew and A. Hidaka and
                      J. R. Huyghe and K. M. Jordahl and J. Morrison and N. Murphy
                      and M. Obón-Santacana and C. M. Ulrich and J. Ose and A. R.
                      Peoples and E. A. Ruiz-Narvaez and A. Shcherbina and M.
                      Stern and Y.-R. Su and F. J. B. van Duijnhoven and V.
                      Arndt$^*$ and J. Baurley and S. I. Berndt and D. T. Bishop
                      and H. Brenner$^*$ and D. D. Buchanan and A. T. Chan and J.
                      C. Figueiredo and S. Gallinger and S. B. Gruber and S.
                      Harlid and M. Hoffmeister$^*$ and M. A. Jenkins and A. D.
                      Joshi and T. O. Keku and S. C. Larsson and L. Le Marchand
                      and L. Li and G. G. Giles and R. L. Milne and H. Nan and R.
                      Nassir and S. Ogino and A. Budiarto and E. A. Platz and J.
                      D. Potter and R. L. Prentice and G. Rennert and L. C. Sakoda
                      and R. E. Schoen and M. L. Slattery and S. N. Thibodeau and
                      B. Van Guelpen and K. Visvanathan and E. White and A. Wolk
                      and M. O. Woods and A. H. Wu and P. T. Campbell and G. Casey
                      and D. V. Conti and M. J. Gunter and A. Kundaje and J. P.
                      Lewinger and V. Moreno and P. A. Newcomb and B. Pardamean
                      and D. C. Thomas and K. K. Tsilidis and U. Peters and W. J.
                      Gauderman and L. Hsu and J. Chang-Claude$^*$},
      title        = {{G}enome-{W}ide {I}nteraction {A}nalysis of {G}enetic
                      {V}ariants with {M}enopausal {H}ormone {T}herapy for
                      {C}olorectal {C}ancer {R}isk.},
      journal      = {Journal of the National Cancer Institute},
      volume       = {114},
      number       = {8},
      issn         = {0027-8874},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2022-01089},
      pages        = {1135-1148},
      year         = {2022},
      note         = {#EA:C020#LA:C020# / 2022 Aug 8;114(8):1135-1148},
      abstract     = {The use of menopausal hormone therapy (MHT) may interact
                      with genetic variants to influence colorectal cancer (CRC)
                      risk.We conducted a genome-wide gene-environment interaction
                      between single nucleotide polymorphisms and the use of any
                      MHT, estrogen-only, and combined estrogen-progestogen
                      therapy with CRC risk, among 28,486 postmenopausal women
                      (11,519 cases and 16,967 controls) from 38 studies, using
                      logistic regression, two-step method, and 2- or
                      3-degree-of-freedom (d.f.) joint test. A set-based score
                      test was applied for rare genetic variants.The use of any
                      MHT, estrogen-only and estrogen-progestogen were associated
                      with a reduced CRC risk [odds ratio (OR) with $95\%$
                      confidence interval $(95\%$ CI) of 0.71 (0.64-0.78), 0.65
                      (0.53-0.79), and 0.73 (0.59-0.90), respectively]. The
                      two-step method identified a statistically significant
                      interaction between a GRIN2B variant rs117868593 and MHT
                      use, whereby MHT-associated CRC risk was significantly
                      reduced in women with the GG genotype [0.68 (0.64-0.72)] but
                      not within strata of GC or CC genotypes. A statistically
                      significant interaction between a DCBLD1 intronic variant at
                      6q22.1 (rs10782186) and MHT use was identified by the 2-d.f.
                      joint test. The MHT-associated CRC risk was reduced with
                      increasing number of rs10782186-C alleles, showing ORs of
                      0.78 (0.70-0.87) for TT, 0.68 (0.63-0.73) for TC, and 0.66
                      (0.60-0.74) for CC genotypes. In addition, five genes in
                      rare variant analysis showed suggestive interactions with
                      MHT (two-sided P < 1.2x10-4).Genetic variants that modify
                      the association between MHT and CRC risk were identified,
                      offering new insights into pathways of CRC carcinogenesis
                      and potential mechanisms involved.},
      cin          = {C020 / C071 / C070 / C120 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331 / I:(DE-He78)C071-20160331 /
                      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:35512400},
      doi          = {10.1093/jnci/djac094},
      url          = {https://inrepo02.dkfz.de/record/180090},
}