Background The underlying cause of epithelial ovarian cancer (EOC) is unknown. It has been theorized that infectious agents could contribute to ovarian tumorigenesis. Objective To investigate the potential role of oncogenic viral infection in EOC, we examined the prevalence of Epstein-Barr Virus (EBV) DNA and cytomegalovirus (CMV) DNA in EOC tissue samples. Methods Formalin-fixed, paraffin-imbedded (FFPE) tumor tissue samples from 198 patients included in the Danish Pelvic Mass Study were studied: 163 with serous adenocarcinomas, 15 with endometrioid adenocarcinomas, 11 with mucinous adenocarcinomas, and nine with clear-cell carcinomas. For controls in the EBV analysis, we used 176 tissue samples from patients diagnosed with benign mucinous cystadenomas. EBV and CMV genotyping was performed by real-time polymerase chain reaction with CMV and EBV CE-IVD approved kits. In-situ hybridization (ISH) was performed on the EBV positive samples. Results Sufficient DNA material was obtained in 191 and 174 tissue samples from cases and controls, respectively. Ten of 191 case samples (5.2%) and one of 174 control samples (0.5%) were positive for EBV DNA ( P value = 0.011). CMV DNA was detected in only one case sample (0.5%). ISH confirmed that three of the samples were of stromal origin, while the remaining seven tested negative for EBV. Conclusions This study is the first to demonstrate a higher prevalence of EBV DNA in tissue samples from patients with EOC than in a benign control group. However, the cellular origin of seven of the samples could not be determined by ISH analysis. Our study did not support an association between CMV and EOC. Electronic supplementary material The online version of this article (10.1186/s13027-019-0223-z) contains supplementary material, which is available to authorized users.

BackgroundThe etiological cause of ovarian cancer is poorly understood. It has been theorized that bacterial or viral infection as well as pelvic inflammatory disease could play a role in ovarian carcinogenesis.AimTo review the literature on studies examining the association between ovarian cancer and bacterial or viral infection or pelvic inflammatory disease.MethodsDatabase search through MEDLINE, applying the medical subject headings: “Ovarian neoplasms”, AND “Chlamydia infections”, “Neisseria gonorrhoeae”, “Mycoplasma genitalium”, “Papillomaviridae”, or “pelvic inflammatory disease”. Corresponding searches were performed in EMBASE, and Web of Science. The literature search identified 935 articles of which 40 were eligible for inclusion in this review.ResultsSeven studies examined the association between bacterial infection and ovarian cancer. A single study found a significant association between chlamydial infection and ovarian cancer, while another study identified Mycoplasma genitalium in a large proportion of ovarian cancer cases. The remaining studies found no association. Human papillomavirus detection rates varied from 0 to 67% and were generally higher in the Asian studies than in studies from Western countries. Cytomegalovirus was the only other virus to be detected and was found in 50% of cases in a case-control study. The association between ovarian cancer and pelvic inflammatory disease was examined in seven epidemiological studies, two of which, reported a statistically significant association.ConclusionsData indicate a potential association between pelvic inflammatory disease and ovarian cancer. An association between ovarian cancer and high-risk human papillomavirus genotypes may exist in Asia, whereas an association in Western countries seems unlikely due to the low reported prevalence. Potential carcinogenic bacteria were found, but results were inconsistent, and further research is warranted.Electronic supplementary materialThe online version of this article (doi:10.1186/s13027-017-0134-9) contains supplementary material, which is available to authorized users.

BackgroundHigh-risk human papillomavirus (HPV) has been suspected to play a role in the carcinogenesis of epithelial ovarian cancer (EOC). However, results from previous studies are conflicting. In most of these studies, the number of tissue samples was small. The current study was therefore undertaken to examine the prevalence of high-risk HPV DNA in EOC in a large series of patients.MethodFormalin-fixed, paraffin-imbedded tumor tissue samples from 198 cases consecutively included in the Danish Pelvic Mass Study were analyzed. The material included 163 serous adenocarcinomas, 15 endometrioid adenocarcinomas, 11 mucinous adenocarcinomas and nine clear-cell carcinomas. Genotyping for high-risk HPV DNA was performed by real-time Polymerase chain reaction (PCR) using an in-house TaqMan singleplex assay targeting the E6/E7 region of the HPV 16 and 18 genomes. Additionally, 20 random samples without HPV 16 and/or 18 infections were reanalyzed for HPV subtypes 31, 33, 35, 39, 45, 51 and 52.ResultsThe quality criteria were fulfilled in 191 samples. HPV 18 DNA was detected in one sample only, while the rest tested negative. The subgroup analysis for seven additional high-risk HPV subtypes was also negative.ConclusionsOnly one in 191 samples was positive for HPV DNA. We therefore conclude that high risk HPV is unlikely to be associated with EOC in a Caucasian population. Future studies should focus on other microorganisms as possible etiological factors in EOC carcinogenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13027-016-0087-4) contains supplementary material, which is available to authorized users.

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