Although it was believed that epithelial ovarian cancers arise from either the surface epithelium of the ovary or from inclusion cysts within the ovary, there is growing evidence to suggest that many, if not most, high-grade serous carcinomas of the ovary arise from the fimbrial end of the fallopian tube rather than from the ovary (4,5). It is suggested that serous epithelial ovarian cancers be separated into two distinct groups—type I and type II serous tumors—as they differ considerably in the cell of origin, molecular pathogenesis, and their biological behavior (6). Type I tumors include serous borderline tumors and low-grade serous carcinoma; they are genetically stable and are characterized by mutations in KRAS and BRAF. Type II serous tumors are rapidly growing, highly aggressive neoplasms that lack well-defined precursor lesions; most are advanced stage at, or soon after, their inception and many appear to arise in the fimbrial end of the fallopian tube (7). The type II tumors are genetically unstable and harbor p53 mutations.
Borderline Tumors An important group of tumors to distinguish is the tumor of low malignant potential, also called the borderline tumor. Borderline tumors are lesions that tend to remain confined to the ovary for long periods, occur predominantly in premenopausal women, and are associated with a very good prognosis (2,3,8–12). They are encountered most frequently in women between the ages of 30 and 50 years, whereas invasive carcinomas occur more often in women between the ages of 50 and 70 years (2).
Although uncommon, implants may occur with serous borderline tumors. Such implants are divided into noninvasive and invasive forms. The latter group has a higher likelihood of developing into progressive, proliferative disease in the peritoneal cavity, which can lead to intestinal obstruction and death (2,6).
Classification of Epithelial Ovarian Tumors Serous Tumors
Serous tumors are so classified because they resemble tubal secretory cells. Psammoma bodies are frequently found in these neoplasms, and they are made up of concentric rings of calcification. Several hypotheses pertaining to the origin and development of psammoma bodies are proposed, including apoptosis of tumor cells and osteoinductive cytokines produced by macrophages (6). In the wall of the mesothelial invaginations, papillary ingrowths are common, representing the early stages of development of a papillary serous cystadenoma. There are many variations in the proliferation of these mesothelial inclusions. Several foci may be lined with ﬂattened inactive epithelium; in adjacent cavities, papillary excrescences are present, often resulting from local irritants (2).
Borderline Serous Tumors Approximately 10% of all ovarian serous tumors fall into the category of a tumor of low malignant potential or borderline tumor (Fig. 37.1), and 50% occur before the age of 40 years. The criteria for the diagnosis of serous borderline tumors are as follows (11): 1.
Epithelial hyperplasia in the form of pseudostratification, tufting, cribriform, and micropapillary architecture 2.
3.
4.
Absence of destructive stromal invasion (i.e., without tissue destruction)
Serous borderline tumors that are composed of an exuberant micropapillary architecture are designated as serous borderline tumors with micropapillary features (Fig. 37.2); these tumors are more frequently bilateral, exophytic, and high-stage than the usual serous borderline tumor.