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Homologous Recombination Deficiency (HRD) is a frequent feature of high-grade epithelial ovarian carcinoma (EOC), associated with sensitivity to PARP-inhibitors (PARPi). The best characterized causes of HRD in EOCs are germline or somatic mutations in <i>BRCA1</i> and <i>BRCA2</i> genes. Although promoter methylation is a well-known mechanism of gene transcriptional repression, few data have been published about <i>BRCA</i> gene methylation in EOCs. In this retrospective study, we quantitatively analyzed by pyrosequencing a selected series of 90 formalin-fixed (FFPE) primary EOCs without <i>BRCA</i> germline mutations. We identified 20/88 (22.7%) EOCs showing <i>BRCA</i> promoter methylation, including 17/88 (19.3%) in <i>BRCA1</i> and 4/86 (4.6%) in <i>BRCA2</i> promoters, one of which showing concomitant <i>BRCA1</i> methylation. Mean methylation levels were 49.6% and 45.8% for <i>BRCA1</i> and <i>BRCA2,</i> respectively, with methylation levels ≥50% in 10/20 methylated EOCs. Constitutive <i>BRCA</i> methylation was excluded by testing blood-derived DNA. In conclusion, pyrosequencing methylation analysis of <i>BRCA</i> genes is a robust, quantitative and sensitive assay applicable to FFPE samples. Remarkably, a considerable subset of germline <i>BRCA</i>-negative EOCs showed somatic methylation and, likely, HRD. A subpopulation of women with <i>BRCA</i> methylation, even without <i>BRCA</i> mutations, could potentially benefit from PARP-inhibitors; further clinical studies are needed to clarify the predictive role of somatic <i>BRCA</i> methylation of PARP-therapy response.