- Early-stage ovarian cancer often presents with vague and ill-defined symptoms.
- Late-stage disease presents with abdominal pain or bloating, early satiety, and/or urinary urgency or frequency.
- The majority of women present with late-stage disease.
- Pelvic ultrasound findings show complex adnexal mass(es).
- The mean age of diagnosis for epithelial ovarian cancer is in the mid-50s, with the majority diagnosed between ages 40 and 65.
- Hereditary causes of ovarian cancer diagnosed at earlier age by almost a decade.
- Nonepithelial ovarian tumors are more common in girls and younger women.
Although there are many different cell types present in the normal adnexa, the majority of adnexal cancers arise from the surface epithelial cells of the ovary (epithelial ovarian cancer [EOC]). Fewer ovarian cancers develop from the remaining cell types (sex cord-stromal, germ cell, or mixed cell type tumors) (Table 50–1), and even fewer adnexal cancers arise from the fallopian tubes, although recent evidence has shown that they account for a greater percentage than previously thought. The specific events leading to the transition of normal tissue to malignancy have not been established, nor has a definitive precursor lesion been identified. For sporadic tumors, molecular events leading to the inactivation of tumor suppressor genes (PTEN, p16, p53) or the activation of oncogenes (HER-2, c-myc, K-ras, Akt) have been described. For the small proportion of genetically heritable cancers, germline mutations in BRCA1, BRCA2, and other genes have been described, but the molecular pathway leading to tumorigenesis has not been elucidated. It is likely that epigenetic events also contribute to the transformation to cancer.
Table 50–1. Categories of Ovarian Cancer. ||Download (.pdf)
Table 50–1. Categories of Ovarian Cancer.
|Epithelial (90%)||Low Malignant Potential||Sex Cord-Stromal (5–8%)||Germ Cell (2–5%)||Metastatic to the Ovary|
|Serous (75–80%)||Serous||Granulosa cell (70%)||Dysgerminoma (30–40%)||Breast|
|Mucinous (10%)||Mucinous||Fibroma||Endodermal sinus tumor||Colon|
|Endometrioid (10%)||Thecoma||Teratoma (immature, mature, specialized)||Stomach|
|Clear cell (1%)||Sertoli-Leydig cell||Embryonal||Endometrium|
|Transitional cell (Brenner's) (1%)||Gynandroblastoma||Choriocarcinoma||Lymphoma|
|Mixed germ cell|
Epithelial Ovarian Cancer
The most prominent theory for the development of EOC associates the repeated trauma and repair to the ovarian epithelium during normal ovulation with subsequent genetic alterations and further progression to malignant transformation. This is supported by evidence that suppression of ovulation leads to a decreased incidence of EOC. A second theory invokes high serum concentrations of gonadotropins, estrogen, androgen, or inflammatory agents, leading to epithelial proliferation and subsequent transformation.
EOCs account for more than 90% of all malignant ovarian tumors and include serous, mucinous, endometrioid, clear cell, transitional cell types, and undifferentiated neoplasms. Serous cystadenocarcinomas represent 75–80% of EOCs. They present with extraovarian spread 85% of the time and are bilateral in half the cases. The tumors are typically large at the time ...