Epithelial ovarian cancer is a malignancy that arises from the cells lining the surface of the ovary, the fallopian tubes, or nearby peritoneal tissue. It accounts for 90% of all ovarian cancers, making it by far the most common type. Despite being grouped under a single name, epithelial ovarian cancer is actually a collection of distinct subtypes that behave very differently, respond to different treatments, and carry different prognoses.
Where Epithelial Ovarian Cancer Starts
For decades, the standard view was that all epithelial ovarian cancers originated from the thin layer of cells covering the ovary’s surface. That view has shifted significantly. Research now shows that the most common and aggressive form, high-grade serous carcinoma, frequently begins not in the ovary itself but in the fimbriae, the finger-like projections at the end of the fallopian tube that sit in close contact with the ovary.
Precancerous changes called serous tubal intraepithelial carcinomas (STICs) have been found in the fallopian tubes of over 70% of women with high-grade serous ovarian cancer, including women with no known genetic predisposition. During ovulation, the ovary’s surface breaks open to release an egg. Abnormal cells from the fallopian tube fimbriae can dislodge during this process, implant on the ovary, and eventually form cysts where cancer develops. This is why preventive removal of the fallopian tubes has become a risk-reduction strategy, and why ovarian, fallopian tube, and peritoneal cancers are now staged under one unified system.
Other subtypes have different origins. Clear cell and endometrioid ovarian cancers are believed to arise from endometriosis, a condition where tissue similar to the uterine lining grows outside the uterus. A subset of mucinous ovarian cancers develops in association with benign ovarian cysts called teratomas.
The Five Major Subtypes
Epithelial ovarian cancer is divided into five main subtypes, each with its own biology and behavior. Understanding which subtype you’re dealing with matters because treatment approaches and expected outcomes differ substantially.
- High-grade serous carcinoma makes up about 68% of all ovarian cancers. It is the most aggressive subtype, grows quickly, and is usually diagnosed at an advanced stage. It tends to develop directly from the fallopian tube or ovarian surface rather than progressing through a slow, stepwise sequence from a benign growth.
- Low-grade serous carcinoma is rare and behaves very differently from its high-grade counterpart. These tumors have few genetic mutations, grow slowly, and follow a more indolent course. They typically develop in a stepwise fashion from precursor lesions.
- Endometrioid carcinoma tends to be slow-growing and is often caught at an earlier stage. It arises from endometriosis and generally carries a better prognosis than high-grade serous disease.
- Clear cell carcinoma also arises from endometriosis. While it is often diagnosed early, it can be more resistant to standard chemotherapy than other subtypes.
- Mucinous carcinoma is relatively uncommon. When truly originating in the ovary (rather than spreading there from elsewhere, such as the gastrointestinal tract), it is often confined to the ovary at diagnosis.
Symptoms and How They Show Up
Epithelial ovarian cancer has a reputation for being “silent,” but most women do experience symptoms, even with early-stage disease. The problem is that those symptoms overlap with common, everyday complaints. In early-stage disease, 51% of women report abdominal pain and 32% report abdominal swelling. In advanced disease, those numbers shift: 62% report swelling and 44% report pain. About 70% of women in both early and advanced stages had symptoms for less than three months before diagnosis.
The pattern to watch for is persistence and frequency. Bloating that doesn’t come and go with meals but lingers day after day, feeling full quickly when eating, pelvic or abdominal pain, and urinary urgency that develops without an obvious cause are the hallmark symptoms. When any of these occur almost daily for two to three weeks and are new for you, that’s the threshold where further evaluation is warranted.
Genetic and Other Risk Factors
Inherited mutations in the BRCA1 and BRCA2 genes are the most significant known risk factors. Women who carry a harmful BRCA1 change have a 39% to 58% lifetime risk of developing ovarian cancer. For BRCA2 carriers, that risk is 13% to 29%. By comparison, the general population lifetime risk is about 1.1%. The difference is dramatic enough that women with these mutations are often offered preventive surgery to remove the ovaries and fallopian tubes.
Other risk factors include a family history of ovarian or breast cancer (even without a known BRCA mutation), increasing age, never having been pregnant, and having used hormone replacement therapy for extended periods. Endometriosis raises the risk of the endometrioid and clear cell subtypes specifically. Factors that suppress ovulation, such as oral contraceptive use and multiple pregnancies, are associated with lower risk.
How It’s Diagnosed
There is no reliable screening test for ovarian cancer in the general population. Diagnosis typically begins when symptoms or an imaging study (usually a pelvic ultrasound) raise suspicion. Blood tests play a supporting role but cannot confirm or rule out the disease on their own.
The most widely used blood marker, CA-125, has significant limitations. It isn’t elevated in roughly half of early-stage ovarian cancers, and it can be elevated in many benign conditions including endometriosis, pelvic inflammatory disease, and even normal menstruation. Its accuracy is notably better in postmenopausal women than in premenopausal women. A newer marker called HE4 has shown better performance, with higher sensitivity (77.5% vs. 69.4%) and higher specificity (96.8% vs. 82.5%) compared to CA-125 in distinguishing malignant from benign ovarian tumors. When the two markers are combined with menopausal status in a scoring system called ROMA, the ability to identify malignancy improves further.
A definitive diagnosis requires tissue sampling, which in most cases happens during surgery. If imaging and blood work strongly suggest ovarian cancer, surgeons often proceed directly to an operation that serves both diagnostic and therapeutic purposes.
Staging
Epithelial ovarian cancer is staged using the FIGO system, which was last updated in 2025. This system now covers ovarian, fallopian tube, and peritoneal cancers under one framework. Stage I means the cancer is confined to the ovaries or fallopian tubes. Stage II indicates spread within the pelvis. Stage III involves spread to the abdominal lining or lymph nodes outside the pelvis, and Stage IV means the cancer has reached distant organs like the liver or lungs or has caused a malignant fluid collection outside the abdomen.
Most women with high-grade serous carcinoma are diagnosed at Stage III or IV, which is a major reason this subtype carries the worst prognosis among the five types.
Treatment: Surgery and Chemotherapy
The standard treatment combines surgery and platinum-based chemotherapy. The order depends on how advanced the cancer is and whether the surgical team believes they can remove enough tumor at the initial operation.
The primary goal of surgery is to remove all visible cancer, a concept called cytoreduction. The benchmark is leaving no tumor deposits larger than 1 cm, but increasingly the target is complete removal with no visible disease remaining (known as R0 resection). In one large study, about 32% of patients achieved R0 at their initial surgery, and those patients had significantly better progression-free and overall survival. When complete removal isn’t feasible upfront, doctors may start with chemotherapy to shrink the cancer first, then perform surgery partway through the treatment course.
After surgery, most women receive several cycles of platinum-based chemotherapy, sometimes combined with a drug that blocks blood vessel growth to tumors. For women whose cancer responds well to this initial treatment, maintenance therapy with PARP inhibitors has become standard of care. PARP inhibitors work by blocking a DNA repair pathway that cancer cells depend on, and they are particularly effective in tumors with BRCA mutations or similar DNA repair deficiencies. This maintenance approach extends the time before cancer returns.
Survival by Stage
Prognosis varies enormously depending on how far the cancer has spread at diagnosis. Based on data from 2015 to 2021, the five-year relative survival rate for localized epithelial ovarian cancer (confined to the ovary) is 92%. For regional disease (spread to nearby structures), it drops to 71%. For distant disease, which is the most common presentation for high-grade serous carcinoma, the five-year survival rate is 32%.
These numbers reflect all women diagnosed during that period and don’t account for newer treatments, particularly PARP inhibitors, which entered wider use during and after that timeframe. Subtype also matters considerably. A woman with early-stage, low-grade serous or endometrioid cancer faces a very different outlook than someone with advanced high-grade serous disease, even though both fall under the umbrella of epithelial ovarian cancer.