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@ARTICLE{Wichert:284415,
      author       = {K. Wichert and R. Hoppe and K. Ickstadt and T. Behrens and
                      S. Winter and R. Herold and C. Terschüren and W.-Y. Lo and
                      P. Guénel and T. Truong and M. K. Bolla and Q. Wang and J.
                      Dennis and K. Michailidou and M. Lush and I. L. Andrulis and
                      H. Brenner$^*$ and J. Chang-Claude$^*$ and A. Cox and S. S.
                      Cross and K. Czene and M. Eriksson and J. D. Figueroa and M.
                      García-Closas and M. S. Goldberg and U. Hamann$^*$ and W.
                      He and B. Holleczek and J. L. Hopper and A. Jakubowska and
                      Y.-D. Ko and J. Lubiński and A. M. Mulligan and N. Obi and
                      V. Rhenius and M. Shah and X.-O. Shu and J. Simard and M. C.
                      Southey and W. Zheng and A. M. Dunning and P. D. P. Pharoah
                      and P. Hall and D. F. Easton and T. Brüning and H.
                      Brauch$^*$ and V. Harth and S. Rabstein},
      title        = {{P}olymorphisms in genes of melatonin biosynthesis and
                      signaling support the light-at-night hypothesis for breast
                      cancer.},
      journal      = {European journal of epidemiology},
      volume       = {38},
      number       = {10},
      issn         = {0393-2990},
      address      = {Dordrecht [u.a.]},
      publisher    = {Springer Science + Business Media B.V.},
      reportid     = {DKFZ-2023-02004},
      pages        = {1053-1068},
      year         = {2023},
      note         = {2023 Oct;38(10):1053-1068},
      abstract     = {Light-at-night triggers the decline of pineal gland
                      melatonin biosynthesis and secretion and is an
                      IARC-classified probable breast-cancer risk factor. We
                      applied a large-scale molecular epidemiology approach to
                      shed light on the putative role of melatonin in breast
                      cancer. We investigated associations between breast-cancer
                      risk and polymorphisms at genes of melatonin
                      biosynthesis/signaling using a study population of 44,405
                      women from the Breast Cancer Association Consortium (22,992
                      cases, 21,413 population-based controls). Genotype data of
                      97 candidate single nucleotide polymorphisms (SNPs) at 18
                      defined gene regions were investigated for breast-cancer
                      risk effects. We calculated adjusted odds ratios (ORs) and
                      $95\%$ confidence intervals (CI) by logistic regression for
                      the main-effect analysis as well as stratified analyses by
                      estrogen- and progesterone-receptor (ER, PR) status. SNP-SNP
                      interactions were analyzed via a two-step procedure based on
                      logic regression. The Bayesian false-discovery probability
                      (BFDP) was used for all analyses to account for multiple
                      testing. Noteworthy associations (BFDP < 0.8) included 10
                      linked SNPs in tryptophan hydroxylase 2 (TPH2) (e.g.
                      rs1386492: OR = 1.07, $95\%$ CI 1.02-1.12), and a SNP in the
                      mitogen-activated protein kinase 8 (MAPK8) (rs10857561: OR =
                      1.11, $95\%$ CI 1.04-1.18). The SNP-SNP interaction analysis
                      revealed noteworthy interaction terms with TPH2- and
                      MAPK-related SNPs (e.g. rs1386483R ∧ rs1473473D ∧
                      rs3729931D: OR = 1.20, $95\%$ CI 1.09-1.32). In line with
                      the light-at-night hypothesis that links shift work with
                      elevated breast-cancer risks our results point to SNPs in
                      TPH2 and MAPK-genes that may impact the intricate network of
                      circadian regulation.},
      keywords     = {Circadian rhythm (Other) / MAPK8 (Other) / Serotonin
                      biosynthesis (Other) / Shift work (Other) / TPH2 (Other)},
      cin          = {C070 / C120 / HD01 / C020 / B072 / TU01},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)C020-20160331 /
                      I:(DE-He78)B072-20160331 / I:(DE-He78)TU01-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37789226},
      doi          = {10.1007/s10654-023-01048-7},
      url          = {https://inrepo02.dkfz.de/record/284415},
}