Article Text

Download PDFPDF
EP874 Serologic markers of Chlamydia trachomatis and other sexually transmitted infections and subsequent ovarian cancer risk: results from the EPIC cohort
  1. A Idahl1,
  2. C Le Cornet2,
  3. S González Maldonado2,
  4. T Waterboer2,
  5. N Bender2,
  6. A Tjønneland3,
  7. L Hansen3,
  8. M-C Boutron-Ruault4,5,
  9. A Fournier4,5,
  10. M Kvaskoff4,5,
  11. H Boeing6,
  12. A Trichopoulou7,
  13. E Valanou7,
  14. E Peppa7,
  15. D Palli8,
  16. C Agnoli9,
  17. A Mattiello10,
  18. R Tumino11,
  19. C Sacerdote12,
  20. C Onland-Moret13,
  21. IT Gram14,
  22. E Weiderpass14,15,16,
  23. JR Quirós17,
  24. EJ Duell18,
  25. M-J Sánchez19,20,
  26. M-D Chirlaque20,21,22,
  27. A Barricarte20,23,24,
  28. L Gil24,
  29. J Brändstedt25,
  30. K Riesbeck26,
  31. E Lundin27,
  32. K-T Khaw28,
  33. A Perez-Cornago29,
  34. M Gunter30,
  35. L Dossus30,
  36. R Kaaks2 and
  37. R Turzanski Fortner2
  1. 1Department of Clinical Sciences, Obstetrics and Gynecology, Umeå University, Umeå, Sweden
  2. 2German Cancer Research Center, Heidelberg, Germany
  3. 3Danish Cancer Society Research Center, Copenhagen, Denmark
  4. 4Université Paris-Saclay
  5. 5Gustave Roussy, Villejuif, France
  6. 6German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany
  7. 7Hellenic Health Foundation, Athens, Greece
  8. 8Institute for Cancer Research, Florence
  9. 9Istituto Nazionale Tumori di Milano Via Venezia, Milan
  10. 10Federico ii University, Naples
  11. 11‘Civic – M.P. Arezzo’ Hospital, Ragusa
  12. 12Città della Salute e della Scienza, Turin, Italy
  13. 13UMC Utrecht, YOUth Onderzoek – Universiteit Utrecht, Utrecht, The Netherlands
  14. 14University of Tromsø, Tromsø
  15. 15Institute of Population-Based Cancer Research, Oslo, Norway
  16. 16Karolinska Institutet, Stockholm, Sweden
  17. 17Conserjeria de Sanidad, Oviedo
  18. 18Catalan Institute of Oncology, Barcelona
  19. 19Hospitales Universitarios de Granada/Universidad de Granada, Granada
  20. 20CIBER in Epidemiology and Public Health, Madrid
  21. 21Regional Health Council, IMIB-Arrixaca
  22. 22Universidad de Murcia, Murcia
  23. 23Navarra Public Health Institute
  24. 24Navarra Institute for Health Research, Pamplona, Spain
  25. 25Lund University, Lund
  26. 26Lund University, Malmö
  27. 27Umeå University, Umeå, Sweden
  28. 28University of Cambridge, Cambridge
  29. 29University of Oxford, Oxford, UK
  30. 30International Agency for Research on Cancer, Lyon, France


Introduction/Background Sexually transmitted infections (STI) and pelvic inflammatory disease may cause damage to the fallopian tube where a substantial proportion of epithelial ovarian cancer (EOC) likely arises. The aim of this study was to determine whether Chlamydia trachomatis antibodies are associated with higher EOC risk. As secondary objectives, we investigated Mycoplasma genitalium,herpes simplex virus type 2 (HSV-2) and human papillomavirus (HPV) 16, 18 and 45 and EOC risk.

Methodology In a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort,791 cases and 1,669 matched controls with pre-diagnosis blood samples were analyzed. Cases and controls were matched on study center, and at blood collection age, time of day, fasting status, exogenous hormone use, menopausal status, and menstrual cycle phase. Antibodies against C. trachomatis, M. genitalium, HSV-2, and HPV 16, 18 and 45 (E6, E7, L1) 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.

Results 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 was associated with higher risk of the mucinous histotype (RR=2.56 [95% CI=1.3–5.05]). Positive serology for chlamydia heat shock protein 60 (cHSP60-1), produced during persistent infection, was associated with higher risk of EOC overall (1.33 [1.09–1.62]) and of the serous subtype (1.42 [1.09–1.84]). None of the other evaluated STIs were associated with EOC risk overall; in analyses by histotype, HSV-2 was associated with higher risk of endometrioid EOC (2.93 [1.50–5.74]).

Conclusion C. trachomatis infection may influence carcinogenesis of serous and mucinous EOC, while HSV-2 might promote endometrioid disease. Mechanisms linking STIs to EOC need to be further elucidated.

Disclosure Financial support: This work was supported by grants from The Cancer Research Foundation in Northern Sweden and The County Council of Västerbotten, Sweden, and the German Cancer Research Center. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by grant givers in the separate countries. Detailed information on demand.

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.