In the United States it is estimated that there will be over 20,000 ovarian cancer cases diagnosed in 2016 leading to over 14,000 deaths, making ovarian cancer the fifth leading contributor to cancer mortality in women. Tumors of the ovary are remarkably varied as they may arise from any of the three cell types in the normal ovary: the multipotent surface (coelomic) epithelium, the totipotent germ cells, and the sex cord–stromal cells. Neoplasms of epithelial origin account for the great majority of ovarian tumors and, in their malignant forms, account for almost 90% of ovarian cancers (
Table 19.3 ). Germ cell and sex cord–stromal cell tumors are much less frequent; although they constitute 20% to 30% of ovarian tumors, they are collectively responsible for less than 10% of malignant tumors of the ovary.
The majority of ovarian tumors arise from the fallopian tube or epithelial cysts in the cortex of the ovary (
Fig.
19.15 ). As mentioned, studies have shown that many of the tumors thought to arise from the coelomic epithelium that covers the surface of the ovary are now thought to arise from the fimbriated end of the fallopian tube (
Fig. 19.15 ). The epithelium lining the cortical cysts may be derived from displaced ovarian surface epithelium or the lining of fallopian tube. These can become metaplastic or undergo neoplastic transformation to give rise to a number of different epithelial tumors. Benign lesions usually are cystic (cystadenoma) and may have an accompanying stromal component (cystadenofibroma). Malignant tumors also may be cystic (cystadenocarcinoma) or solid (carcinoma).
http://ebooksmedicine.net
Table 19.3 Frequency of Major Ovarian Tumors
Some ovarian epithelial tumors fall into an intermediate category currently referred to as borderline tumors. Although the majority of borderline tumors behave in a benign manner they can recur and some can progress to carcinoma.
Important risk factors for ovarian cancer include nulliparity, family history, and germline mutations in certain
Fig. 19.15 Derivation, of various ovarian neoplasms. Type I tumors progress from benign tumors through borderline tumors that may give rise to a low-grade carcinoma. Type II tumors arise from inclusions cysts/fallopian tube epithelium via intraepithelial precursors that are often not identified. They demonstrate high-grade features and are most commonly of serous histology. STIC, serous tubal intraepithelial carcinoma.
tumor suppressor genes. There is a higher incidence of carcinoma in unmarried women and married women with low parity. Of interest, prolonged use of oral contraceptives reduces the risk. Around 5% to 10% of ovarian cancers are familial, and most of these are associated with mutations in the BRCA1 or BRCA2 tumor suppressor genes. As will be discussed later, mutations in BRCA1 and BRCA2 also are associated with hereditary breast cancer. The average lifetime risk for ovarian cancer is approximately 30% in BRCA1 carriers; the risk in BRCA2 carriers is somewhat lower. In contrast with familial ovarian cancer, mutations in BRCA1 and BRCA2 are found in only 8% to 10% of sporadic ovarian cancers, which appear to arise through alternative molecular mechanisms.