Epithelial Ovarian CancerEdit
Epithelial ovarian cancer refers to a group of malignancies arising from the surface epithelium of the ovary, with the majority of ovarian cancers falling into this category. It is the leading cause of death from gynecologic cancers in many populations due to its tendency to grow silently and be diagnosed at an advanced stage. Over the past decades, advances in surgery, chemotherapy, and targeted therapies have improved outcomes for many patients, while ongoing debates about screening, genetic testing, and access to care continue to shape policy and practice. For orientation, see ovarian cancer and the specific entity epithelial ovarian cancer.
Most epithelial ovarian cancers are high-grade serous carcinomas, but the category also includes endometrioid, clear cell, mucinous, and other histologies. The disease commonly presents at an advanced stage, where extensive peritoneal spread is typical. Early detection remains a challenge because symptoms—bloating, abdominal discomfort, pelvic fullness—are vague and easily attributed to benign conditions. The standard treatment paradigm emphasizes maximal tumor debulking through surgery, when feasible, followed by platinum-based chemotherapy. For patients with certain genetic alterations, modern targeted therapies offer additional options. See high-grade serous carcinoma for the most common histology, endometrioid carcinoma for another subtype, and parp inhibitors for agents used in selected cases.
Epidemiology and risk factors
Epithelial ovarian cancer is relatively uncommon compared with other cancers but carries a disproportionate mortality burden among gynecologic cancers. Age is a major risk factor, with incidence rising after menopause, but inherited predispositions can accelerate onset. Pathogenic variants in BRCA1 and BRCA2 markedly increase lifetime risk and influence treatment choices; individuals with these mutations may benefit from targeted prevention and therapy strategies. Other hereditary syndromes, such as Lynch syndrome, also modify risk. Protective factors include use of oral contraceptives, pregnancy, and tubal history that reduces exposure of ovarian tissue to potential carcinogenic events, though these do not guarantee prevention. See risk factors for ovarian cancer for more detail.
Environmental, reproductive, and lifestyle factors interact with biology to shape risk. A substantial portion of risk is linked to tissue biology and genomic instability, including alterations in homologous recombination pathways. When present, these features guide the use of targeted therapies such as PARP inhibitors and influence prognostic considerations. For a discussion of genetic testing and risk assessment, see genetic testing in ovarian cancer and BRCA1/BRCA2.
Pathogenesis and histology
The disease most often begins in the epithelial linings covering the ovary, but mounting evidence points to a substantial proportion of high-grade serous cancers originating in the fimbrial end of the fallopian tube and shedding pigment or cells onto the ovarian surface. This tubal-origin theory has shifted thinking about early detection and prevention strategies, especially for high-risk individuals. The major histologic groups within epithelial ovarian cancer include: - high-grade serous carcinoma - endometrioid carcinoma - clear cell carcinoma - mucinous carcinoma - others
High-grade serous carcinoma is the most common and is frequently associated with defects in DNA repair pathways, particularly with BRCA1/BRCA2 mutations and broader HRD (homologous recombination deficiency) status. The molecular landscape informs both prognosis and treatment decisions, including responsiveness to platinum chemotherapy and sensitivity to PARP inhibitors like olaparib and related agents. For more on histology, see high-grade serous carcinoma, endometrioid carcinoma, and clear cell carcinoma.
Clinical presentation, diagnosis, and staging
Symptoms are often nonspecific and may reflect peritoneal involvement (bloating, early satiety, abdominal pain, urinary urgency). Because of this, most cases are diagnosed at an advanced stage, where treatment aims to reduce tumor burden and control disease. Diagnostic workup typically includes physical examination, imaging such as pelvic ultrasonography and cross-sectional imaging, biomarkers like CA-125 and, increasingly, other markers (e.g., HE4), and, when appropriate, genetic testing. See CA-125 and HE4 for biomarker context.
Staging follows international guidelines, commonly the FIGO system (the FIGO staging system), which informs prognosis and treatment planning. Imaging and surgical assessment help determine the extent of disease and the feasibility of complete cytoreduction, a central goal of initial management. In selected cases, neoadjuvant chemotherapy may be used when upfront surgery would be technically challenging or unsafe. See FigO staging for more on staging conventions and surgical cytoreduction for the surgical approach.
Treatment and outcomes
The backbone of treatment is aggressive surgical cytoreduction (often termed debulking) followed by platinum-based chemotherapy, typically a platinum compound (carboplatin) with a taxane (paclitaxel). The goal is no visible residual disease or as little as possible, as residual tumor burden correlates with survival. For patients with BRCA1/BRCA2 mutations or other forms of homologous recombination deficiency, adding targeted therapies can improve progression-free survival and, in some settings, overall survival. Examples include PARP inhibitors and anti-angiogenic agents such as bevacizumab in certain regimens.
Emerging approaches emphasize individualization of therapy based on tumor biology, including HRD testing and genomic profiling. For patients with recurrent disease, options depend on prior treatment and platinum sensitivity, with defined lines of chemotherapy and targeted therapies remaining under active investigation in clinical trials. See olaparib for a commonly used PARP inhibitor and bevacizumab for anti-angiogenic strategy.
Risk reduction, screening, and genetic testing
Strategies to reduce risk are particularly relevant for individuals with inherited risk. For those with BRCA1/BRCA2 mutations or strong family history, risk-reducing bilateral salpingo-oophorectomy significantly lowers cancer risk and is a standard counseling point in appropriate age windows. The decision involves balancing cancer risk reduction with potential effects on fertility and hormonal status. See risk-reducing salpingo-oophorectomy and BRCA1/BRCA2.
Screening for epithelial ovarian cancer in average-risk populations has not demonstrated a clear mortality benefit and is not routinely recommended. Guidelines emphasize careful evaluation of symptoms, risk-based testing, and targeted surveillance in high-risk groups. Genetic testing and counseling are important components of care for individuals with familial risk, guiding both prevention and treatment decisions. See screening for ovarian cancer and genetic testing in ovarian cancer.
Controversies and debates
Policy debates surrounding ovarian cancer care frequently touch on access, cost, and optimal use of scarce health-care resources. A market-oriented frame emphasizes patient choice, price transparency, and evidence-based allocation of funds toward interventions with proven benefit, while resisting mandates that could drive higher costs or restrict private options. Proponents argue that focusing resources on high-risk populations (e.g., those with BRCA mutations) and supporting innovation through private investment yields better outcomes than broad, universal mandates for screening or testing. Critics of this stance describe concerns about disparities and advocate for broader access to genetic counseling, targeted screening where evidence supports it, and protections against financial hardship in cancer care. In this discourse, some critics label certain policy positions as “woke” activism, arguing that they overemphasize social equity in ways that may inflate costs or delay proven treatments; supporters respond that equity considerations are essential to timely and effective care. The practical takeaway is that ongoing research, cost-benefit analyses, and patient-centered decision making guide policy as well as clinical guidelines. See healthcare policy and cost-effectiveness analysis for related discussions.