The Clinicopathological Basis Of The Proposed Model

In the last several years, attempts have been made to characterize the clinicopatho-logical features of noninvasive and invasive epithelial ovarian tumors of all histological types in an effort to elucidate their pathogenesis and behavior (2,7-9). These studies identified a subset of low-grade serous tumors originally designated "micropapillary serous carcinoma (MPSC)" with characteristic histopathological features, low proliferative activity, and an indolent behavior. These tumors contrast dramatically with the conventional type of serous carcinoma, which is a high-grade aggressive neoplasm that has high proliferative activity (2,7,9). The term "MPSC" was originally proposed to distinguish the noninvasive form of this tumor from the more common noninvasive tumor, termed an "atypical proliferative serous tumor," both of which have been included under the rubric of "borderline" or "low-malignant potential" (7,9). Subsequent studies have suggested that MPSC is the precursor or in situ lesion of invasive low-grade serous carcinoma and therefore, the term "intraepithelial low-grade serous carcinoma" is preferred. Histological transitions from cystadenoma/adenofibromas and atypical proliferative serous tumors to intraepithelial low-grade serous carcinomas are observed in nearly 75% of cases (10). In addition, areas of infiltrative growth (stromal invasion) immediately adjacent to the intraepithelial component are found in a significant proportion of cases (10). The aforementioned histopathological findings strongly suggest that there is a spectrum of tumor progression beginning with a benign serous cystadenoma/adenofibroma, through a proliferative tumor (atypical proliferative serous tumor) to an intraepithelial low-grade serous carcinoma and finally, to an invasive low-grade serous carcinoma.

Usually, patients with low-grade serous carcinomas have an indolent course that might last as long as 20 years (9,10). Approximately 50% of patients with low-grade serous carcinoma ultimately succumb to their disease because of widespread intraabdominal carcinomatosis. But the tumor generally maintains its low-grade appearance and low proliferative index throughout its course (10). This contrasts with high-grade serous carcinoma, which presents as an aggressive neoplasm that spreads rapidly and is associated with a poor outcome. Analysis of nonserous ovarian tumors including muci-nous, endometrioid, clear cell carcinomas, and malignant Brenner tumors reveal that they are often associated with cystadenomas, borderline tumors, and intraepithelial carcinomas (2). Furthermore, it has been long recognized that endometrioid carcinoma and clear cell carcinoma are associated with endometriosis in the ovary or pelvis in 15-50% of cases (11,12). This finding suggests that endometriosis is a precursor of these tumors. In parallel with the aforementioned clinical observation, a recent transvaginal ultrasonography study has shown that approx 50% of ovarian carcinomas develop from pre-existing cystic lesions, whereas the remaining 50% develop in ovaries without an apparent abnormality on ultrasound (13). The former group was mainly made up of mucinous, endometrioid, clear cell carcinomas, and borderline tumors, whereas the latter group was made up almost exclusively of high-grade serous carcinomas. This distribution corresponds to the type I and type II tumors.

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