Ovarian cancers pose the greatest challenge for gynecological oncology. They are a heterogeneous, rapidly progressing and highly lethal group of malignancies and their etiology is still poorly understood. Among many hypotheses, explaining the pathogenesis of malignant tumors, chronic inflammation seems to play a significant role, which was proved in cervical, hepatic and esophageal cancers. The processes of inflammation and carcinogenesis are very much alike. Their similarity was experimentally confirmed by epidemiological, immunological, biochemical and genetic studies. Additionally, this view is supported by indirect epidemiological and clinical evidence linking ovarian cancer with pelvic inflammatory disease, endometriosis or polycystic ovary syndrome. Chronic inflammation is a key factor in the pathogenesis of these illnesses. Moreover, ovulation involving repeated damage and repair of the ovarian surface epithelium is in fact an inflammatory process. In this review, we focus on the role of inflammation in cancer initiation, promotion and progression with special emphasis on the ovarian cancer. We discuss the potential involvement of the fallopian tubes, endometriosis and microenvironment of tumors represented by cytokines, chemokines, growth factors and various enzymes that destroy the extracellular matrix. Considering that molecular biology is currently rapidly evolving, we focus on the function of the mammalian target of rapamycin (mTOR) kinase and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in the pathophysiology of inflammation and cancer.