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@ARTICLE{Labadie:163159,
      author       = {J. D. Labadie and T. A. Harrison and B. Banbury and E. L.
                      Amtay and S. Bernd and H. Brenner$^*$ and D. D. Buchanan and
                      P. T. Campbell and Y. Cao and A. T. Chan and J.
                      Chang-Claude$^*$ and D. English and J. C. Figueiredo and S.
                      J. Gallinger and G. G. Giles and M. J. Gunter and M.
                      Hoffmeister$^*$ and L. Hsu and M. A. Jenkins and Y. Lin and
                      R. L. Milne and V. Moreno and N. Murphy and S. Ogino and A.
                      I. Phipps and L. C. Sakoda and M. L. Slattery and M. C.
                      Southey and W. Sun and S. N. Thibodeau and B. Van Guelpen
                      and S. H. Zaidi and U. Peters and P. A. Newcomb},
      title        = {{P}ostmenopausal {H}ormone {T}herapy and {C}olorectal
                      {C}ancer {R}isk by {M}olecularly {D}efined {S}ubtypes and
                      {T}umor {L}ocation.},
      journal      = {JNCI cancer spectrum},
      volume       = {4},
      number       = {5},
      issn         = {2515-5091},
      address      = {Oxford},
      publisher    = {Oxford University Press},
      reportid     = {DKFZ-2020-01862},
      pages        = {pkaa042},
      year         = {2020},
      abstract     = {Postmenopausal hormone therapy (HT) is associated with a
                      decreased colorectal cancer (CRC) risk. As CRC is a
                      heterogeneous disease, we evaluated whether the association
                      of HT and CRC differs across etiologically relevant,
                      molecularly defined tumor subtypes and tumor location.We
                      pooled data on tumor subtypes (microsatellite instability
                      status, CpG island methylator phenotype status, BRAF and
                      KRAS mutations, pathway: adenoma-carcinoma, alternate,
                      serrated), tumor location (proximal colon, distal colon,
                      rectum), and HT use among 8220 postmenopausal women (3898
                      CRC cases and 4322 controls) from 8 observational studies.
                      We used multinomial logistic regression to estimate odds
                      ratios (OR) and $95\%$ confidence intervals (CIs) for the
                      association of ever vs never HT use with each tumor subtype
                      compared with controls. Models were adjusted for study, age,
                      body mass index, smoking status, and CRC family history. All
                      statistical tests were 2-sided.Among postmenopausal women,
                      ever HT use was associated with a $38\%$ reduction in
                      overall CRC risk (OR =0.62, $95\%$ CI = 0.56 to 0.69). This
                      association was similar according to microsatellite
                      instability, CpG island methylator phenotype and BRAF or
                      KRAS status. However, the association was attenuated for
                      tumors arising through the serrated pathway (OR = 0.81,
                      $95\%$ CI = 0.66 to 1.01) compared with the
                      adenoma-carcinoma pathway (OR = 0.63, $95\%$ CI = 0.55 to
                      0.73; Phet =.04) and alternate pathway (OR = 0.61, $95\%$
                      CI = 0.51 to 0.72). Additionally, proximal colon tumors had
                      a weaker association (OR = 0.71, $95\%$ CI = 0.62 to 0.80)
                      compared with rectal (OR = 0.54, $95\%$ CI = 0.46 to 0.63)
                      and distal colon (OR = 0.57, $95\%$ CI = 0.49 to 0.66;
                      Phet =.01) tumors.We observed a strong inverse association
                      between HT use and overall CRC risk, which may predominantly
                      reflect a benefit of HT use for tumors arising through the
                      adenoma-carcinoma and alternate pathways as well as distal
                      colon and rectal tumors.},
      cin          = {C070 / C120 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)C020-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32923935},
      pmc          = {pmc:PMC7477374},
      doi          = {10.1093/jncics/pkaa042},
      url          = {https://inrepo02.dkfz.de/record/163159},
}