Ovarian cancer is a malignancy arising from the ovaries or adjacent fallopian tubes. Although not the most common gynecologic cancer — that distinction belongs to endometrial cancer — ovarian cancer is by far the most lethal, causing more deaths than all other gynecologic cancers combined. The reason is its characteristic silent early course: symptoms are vague and nonspecific until the disease has spread throughout the peritoneal cavity, at which point over 75% of cases are diagnosed at advanced stage. Early detection, aided by modern imaging, significantly improves outcomes.
Understanding ovarian cancer requires knowing what it is — and what it is not. The majority of ovarian masses are benign: simple ovarian cysts, hemorrhagic functional cysts, endometriomas, dermoid cysts, and cystadenomas all require careful MRI characterization to distinguish from malignancy. Endometriosis is an independent risk factor for two specific ovarian cancer subtypes — endometrioid and clear cell carcinoma. Women with BRCA mutations also carry elevated endometrial cancer and breast cancer risk, and Lynch syndrome elevates both ovarian and endometrial cancer risk simultaneously.
Causes
Genetic and hereditary factors.
Approximately 15–20% of all ovarian cancers are caused by inherited germline mutations, making ovarian cancer one of the most hereditary of all solid tumors. BRCA1 mutations confer a lifetime ovarian cancer risk of approximately 40–46%, and BRCA2 mutations confer a risk of approximately 12–20% — compared to the 1.2% population lifetime risk. Lynch syndrome (mismatch repair gene deficiency) elevates ovarian cancer risk to approximately 10–12% lifetime. Women with a personal or family history of ovarian, breast, colorectal, or endometrial cancer should be offered genetic counseling and testing, as identification of a germline mutation profoundly changes screening, prevention, and treatment decisions. The high-grade serous subtype — the most common and lethal — is the ovarian cancer most strongly associated with BRCA mutations, and is now understood to arise predominantly from the fimbriated end of the fallopian tube rather than the ovarian surface itself, fundamentally changing our understanding of ovarian cancer biology.
Other risk factors.
The shared biology of ovarian cancer with uninterrupted ovulation is supported by the fact that any condition or intervention that reduces lifetime ovulation cycles reduces risk: pregnancy, breastfeeding, and long-term combined oral contraceptive use are all associated with 30–60% risk reduction, with greater protection accruing with more pregnancies and longer OCP duration. Conversely, nulliparity, infertility, and fertility treatment increase risk. Advancing age — most cases occur after menopause, with peak incidence in the 60s — is the single strongest risk factor after genetics. Endometriosis is associated with a 2–3 fold increased risk of endometrioid and clear cell ovarian carcinoma specifically. Postmenopausal hormone replacement therapy with estrogen alone modestly increases risk. Obesity elevates risk, particularly for endometrioid and clear cell subtypes.
Symptoms
Ovarian cancer earned its description as the "silent killer" because Stage I disease — when cure rates exceed 90% — produces no symptoms in the majority of cases, and Stage III–IV disease — present at diagnosis in over 75% of patients — produces symptoms so nonspecific that months typically elapse between their onset and diagnosis. The symptoms of advanced ovarian cancer are driven by peritoneal spread and ascites: persistent abdominal bloating or distension (the single most common symptom), pelvic or abdominal pain, early satiety and difficulty eating a full meal, urinary urgency or frequency from bladder compression, and unexplained fatigue, back pain, and unintentional weight loss. The critical clinical rule is persistence: these symptoms occurring nearly every day for more than 2–3 weeks without an obvious benign explanation require pelvic examination and imaging. Menstrual irregularities may occur when the cancer or its associated ascites disrupts normal ovarian function. Postmenopausal vaginal bleeding from the associated endometrial abnormalities that can accompany certain ovarian cancer subtypes occasionally prompts evaluation.
Diagnosis
Evaluation begins with pelvic examination and transvaginal ultrasound, which identifies ovarian masses and assesses their morphology. The IOTA (International Ovarian Tumor Analysis) ultrasound classification rules — including the simple rules and ADNEX model — provide validated risk stratification based on ultrasound features. Tumor markers including CA-125 (elevated in approximately 80% of epithelial ovarian cancers but lacking specificity in premenopausal women), HE4 (human epididymis protein 4), and the ROMA score combining CA-125 and HE4 are measured when ovarian malignancy is suspected.
An MRI of the pelvis is the most accurate noninvasive imaging study for characterizing adnexal masses and is the preferred modality for risk stratification when ultrasound findings are equivocal or complex. The O-RADS MRI scoring system (1–5) provides standardized, validated characterization based on the presence of enhancing solid components, papillary projections with gadolinium enhancement, thick irregular septations, restricted diffusion on DWI, and peritoneal disease — features that distinguish malignant from benign masses with accuracy exceeding 90%. MRI is particularly valuable for evaluating the primary tumor extent, identifying involvement of the uterus, parametria, bladder, and rectosigmoid, and detecting peritoneal implants accessible to primary debulking surgery vs. those requiring neoadjuvant chemotherapy first. CT of the chest, abdomen, and pelvis is the standard staging imaging modality — evaluating lymph node involvement, liver and splenic parenchymal metastases, pleural effusion, and the distribution of peritoneal disease. PET-CT provides metabolic staging and is increasingly used to evaluate response to treatment and detect recurrence.
Classification
Ovarian cancers are classified by cell of origin — which determines biology, prognosis, and treatment — and staged by the FIGO system.
By cell type:
- Epithelial ovarian cancer (90%): Arises from the surface epithelium of the ovary or fallopian tube. Subtypes include high-grade serous carcinoma (the most common and lethal subtype, strongly associated with BRCA mutations and fallopian tube origin), low-grade serous carcinoma (less aggressive, different biology and treatment), endometrioid carcinoma (associated with endometriosis and Lynch syndrome), clear cell carcinoma (associated with endometriosis, particularly chemotherapy-resistant), and mucinous carcinoma (often large, unilateral, frequently secondaries from GI primary).
- Germ cell tumors: Arise from egg-producing cells; more common in women under 30. Includes dysgerminoma (the most common malignant germ cell tumor, highly chemosensitive) and immature teratoma. Often curable even at advanced stage with combination chemotherapy.
- Sex cord-stromal tumors: Arise from the supporting stromal cells of the ovary. Granulosa cell tumors produce estrogen and may cause postmenopausal bleeding or precocious puberty. Sertoli-Leydig tumors produce androgens and may cause virilization. Generally low-grade with favorable prognosis.
By FIGO stage:
- Stage I: Cancer confined to one (IA) or both (IB) ovaries or fallopian tubes, or with capsule rupture or malignant ascites (IC). Five-year survival greater than 90% when completely resected.
- Stage II: Cancer has spread to other pelvic structures including the uterus, fallopian tubes, or peritoneum. Five-year survival approximately 70%.
- Stage III: Cancer has spread beyond the pelvis to the abdominal peritoneum (IIIA/B) or to regional lymph nodes (IIIC). The most common stage at diagnosis for high-grade serous carcinoma. Five-year survival 25–50% depending on substage and completeness of debulking.
- Stage IV: Cancer has spread to the liver or splenic parenchyma (IVA) or to distant organs including lungs, pleura, or supraclavicular nodes (IVB). Five-year survival approximately 17%.
Treatments
Treatment is tailored to cancer type, FIGO stage, and individual patient factors including fitness for surgery and genetic profile.
Surgery (cytoreductive debulking): Surgery is the cornerstone of treatment for most ovarian cancers. The goal of primary cytoreductive surgery — also called debulking — is complete resection of all visible tumor (R0 resection), as the amount of residual disease after surgery is the single strongest predictor of survival. Standard procedures include total hysterectomy, bilateral salpingo-oophorectomy, omentectomy, pelvic and para-aortic lymph node sampling, and resection of all peritoneal implants. Upper abdominal procedures including splenectomy, bowel resection, and diaphragm stripping may be required to achieve complete cytoreduction. Primary debulking surgery is performed upfront when complete or near-complete resection is achievable; interval debulking surgery — after neoadjuvant chemotherapy — is used when the disease burden is too extensive for upfront resection.
Chemotherapy.
Carboplatin and paclitaxel administered intravenously is the standard first-line regimen for most epithelial ovarian cancers, typically delivered for 6 cycles. Intraperitoneal (IP) chemotherapy — delivering drug directly into the peritoneal cavity through a surgically placed port — improves survival in appropriately selected patients with Stage III disease but is associated with greater toxicity. Neoadjuvant chemotherapy (3 cycles before surgery, 3 cycles after) is used when primary complete debulking is not feasible, or when the patient cannot tolerate upfront surgery.
Targeted therapy and maintenance treatment.
PARP inhibitors — olaparib, niraparib, rucaparib — have transformed the treatment of ovarian cancer by exploiting the DNA repair deficiency in BRCA-mutated and homologous recombination-deficient tumors. Maintenance PARP inhibitor therapy after response to first-line chemotherapy significantly delays recurrence, with the greatest benefit in BRCA mutation carriers. Bevacizumab (anti-VEGF antibody) combined with chemotherapy and continued as maintenance improves progression-free survival in advanced disease. Testing for BRCA mutations and homologous recombination deficiency is now standard at diagnosis to guide maintenance therapy selection.
Fertility-sparing treatment.
In carefully selected young women with Stage IA, Grade 1 epithelial cancer or early-stage germ cell tumors, unilateral salpingo-oophorectomy preserving the uterus and contralateral ovary may be possible, followed by standard chemotherapy when indicated. This decision requires expert multidisciplinary planning at a specialized center.
Risk reduction for high-risk women.
Women with confirmed BRCA1 or BRCA2 mutations who have completed childbearing are strongly recommended to undergo risk-reducing bilateral salpingo-oophorectomy (RRBSO), which reduces ovarian cancer risk by over 95% and also reduces breast cancer risk. The optimal timing is age 35–40 for BRCA1 carriers and 40–45 for BRCA2 carriers. Annual screening with CA-125 and transvaginal ultrasound in high-risk women who have not yet undergone RRBSO is recommended, though its effectiveness for early detection is limited.
Get an MRI to Confirm Your Diagnosis
Before surgical planning or starting treatment, a clear MRI diagnosis ensures the right path forward. First Look MRI offers self-pay Pelvis MRI scans — no doctor's order or insurance required — at our locations in Georgia, Texas, and Colorado.