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In this controlled study, we aimed to evaluate the sexual dysfunction of patients with polycystic ovary syndrome (PCOS) in comparison to healthy controls. We enrolled 64 sexually active women in our study. The PCOS group consisted of 32 women who met the Rotterdam diagnostic criteria, and the control group was composed of 32 age-matched, healthy females. In addition to the demographic and clinical characteristics of the participants, the hormonal and biochemical parameters were also studied. All patients were invited to fill out the female sexual function index (FSFI) and Beck's Depression Inventory questionnaires. The prevalence of sexual dysfunction in the PCOS group was similar to controls (25% vs 19%; P=0.54). No significant difference was found according to each domain score of FSFI. Significant negative correlations were found between the total FSFI scores of the PCOS group and the total (r=-0.278) and free testosterone (r=-0.493) levels. Although depressive scores of PCOS patients were higher, they did not show greater impaired sexual functions than age-matched controls according to their FSFI scores. Considering the multifactorial state of female sexual dysfunction, further studies are needed to clarify the impact of PCOS upon sexuality.

Aberrant methylation of gene promoter regions is one of the mechanisms for inactivation of tumor suppressor genes in human malignancies. In this study, the methylation pattern of 24 tumor suppressor genes was analyzed in 75 samples of ovarian cancer using the methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) assay. Of the 24 tumor suppressor genes examined, aberrant methylation was observed in 17. The three most frequently methylated genes were CDKN2B, CDH13 and RASSF1, followed by ESR1 and MLH1. Methylation frequencies ranged from 1.3% for CDKN2A, RARβ, CASP8, VHL and TP73 to 24% for CDKN2B. The corresponding normal DNA from each patient was also investigated. Methylation was detected in tumors, although not in normal tissues, with the exception of two samples, indicating aberrant methylation in tumors. Clear cell carcinoma samples exhibited a higher frequency of CDKN2B promoter hypermethylation compared to those of other histological types (P=0.05). Our data indicate that methylation of the CDKN2B gene is a frequent event in ovarian carcinogenesis and that analysis of only three genes is sufficient to detect the presence of methylation in 35% of ovarian cancer cases. However, more studies using a much larger sample size are needed to define the potential role of DNA methylation as a marker for ovarian cancer.

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