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@ARTICLE{Idahl:154416,
      author       = {A. Idahl and C. L. Cornet$^*$ and S. G. Maldonado$^*$ and
                      T. Waterboer$^*$ and N. Bender$^*$ and A. Tjønneland and L.
                      Hansen and M.-C. Boutron-Ruault and A. Fournier and M.
                      Kvaskoff and H. Boeing and A. Trichopoulou and E. Valanou
                      and E. Peppa and D. Palli and C. Agnoli and A. Mattiello and
                      R. Tumino and C. Sacerdote and N. C. Onland-Moret and I. T.
                      Gram and E. Weiderpass and J. R. Quirós and E. J. Duell and
                      M.-J. Sánchez and M.-D. Chirlaque and A. Barricarte and L.
                      Gil and J. Brändstedt and K. Riesbeck and E. Lundin and
                      K.-T. Khaw and A. Perez-Cornago and M. J. Gunter and L.
                      Dossus and R. Kaaks$^*$ and R. Turzanski-Fortner$^*$},
      title        = {{S}erologic markers of {C}hlamydia trachomatis and other
                      sexually transmitted infections and subsequent ovarian
                      cancer risk: {R}esults from the {EPIC} cohort.},
      journal      = {International journal of cancer},
      volume       = {147},
      number       = {8},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2020-00747},
      pages        = {2042-2052},
      year         = {2020},
      note         = {147(8):2042-2052#LA:C020#},
      abstract     = {A substantial proportion of epithelial ovarian cancer (EOC)
                      arises in the fallopian tube and other epithelia of the
                      upper genital tract; these epithelia may incur damage and
                      neoplastic transformation following sexually transmitted
                      infections (STI) and pelvic inflammatory disease. We
                      investigated the hypothesis that past STI infection,
                      particularly Chlamydia trachomatis, is associated with
                      higher EOC risk in a nested case-control study within the
                      European Prospective Investigation into Cancer and Nutrition
                      (EPIC) cohort including 791 cases and 1,669 matched
                      controls. Serum antibodies against C. trachomatis,
                      Mycoplasma genitalium, herpes simplex virus type 2 (HSV-2)
                      and human papillomavirus (HPV) 16, 18 and 45 were assessed
                      using multiplex fluorescent bead-based serology. Conditional
                      logistic regression was used to estimate relative risks (RR)
                      and $95\%$ confidence intervals [CI] comparing women with
                      positive vs. negative serology. A total of $40\%$ of the
                      study population was seropositive to at least one STI.
                      Positive serology to C. trachomatis Pgp3 antibodies was not
                      associated with EOC risk overall, but with higher risk of
                      the mucinous histotype (RR=2.30 $[95\%$ CI=1.22-4.32]).
                      Positive serology for chlamydia heat shock protein 60
                      (cHSP60-1) was associated with higher risk of EOC overall
                      (1.36 [1.13-1.64]) and with the serous subtype (1.44
                      [1.12-1.85]). None of the other evaluated STIs were
                      associated with EOC risk overall; however, HSV-2 was
                      associated with higher risk of endometrioid EOC (2.35
                      [1.24-4.43]). The findings of this study suggest a potential
                      role of C. trachomatis in the carcinogenesis of serous and
                      mucinous EOC, while HSV-2 might promote the development of
                      endometrioid disease.},
      subtyp        = {Review Article},
      cin          = {C020 / F022 / F020},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331 / I:(DE-He78)F022-20160331 /
                      I:(DE-He78)F020-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32243586},
      doi          = {10.1002/ijc.32999},
      url          = {https://inrepo02.dkfz.de/record/154416},
}