Clinical and Pathologic Observations Supporting the Dualistic Ovarian Carcinogenesis Model

Comprehensive efforts have been made in analyzing histopathologic and clinical features of a large number of noninvasive and invasive epithelial ovarian tumors to delineate their pathogenesis and behavior.1,9-11 One of the main conclusions from these studies is the recognition of a subset of low-grade serous tumors designated micropapillary serous carcinoma (MPSC), which displays characteristic histopatho-logic features, low proliferative activity, and an indolent behavior that contrasts dramatically with the conventional type of serous carcinoma.1,9-11 The term MPSC was originally proposed by Dr. Kurman and colleagues to distinguish this tumor from the more common noninvasive tumor, termed an atypical proliferative serous tumor, both of which have been classified as borderline or low malignant potential tumor.9,11 Histologic transitions from adenofibromas and atypical proliferative serous tumors to noninvasive MPSCs are observed and areas of infiltrative growth (stromal invasion) immediately adjacent to the noninvasive component are found in a significant proportion of cases.12 Subsequent studies have suggested that these invasive MPSCs are synonymous with invasive low-grade serous carcinoma. The histopathologic findings suggest a morphologic and biologic spectrum of tumor progression beginning from a benign serous cystadenoma/adenofibroma through a proliferative tumor (atypical proliferative serous tumor) to a noninvasive low-grade carcinoma (noninvasive MPSC), and ending with an invasive low-grade serous carcinoma (invasive MPSC).

In contrast to conventional high-grade serous carcinoma that is a clinically aggressive neoplasm, invasive low-grade serous carcinomas typically pursue a relatively indolent course that may go on for years.11,12 Approximately 50% to 60% of patients with invasive low-grade carcinomas ultimately succumb to their disease because of widespread intra-abdominal carcinomatosis, but the tumor maintains its low-grade appearance and low proliferative activity throughout its clinical course.12 Analyses of mucinous, endometrioid, clear cell carcinomas, and malignant Brenner tumors reveal that they are often associated with cystadenomas, borderline tumors, and intraepithelial carcinomas.1 Furthermore, it has been long recognized that endome-trioid carcinoma and clear cell carcinoma are associated with endometriosis in the ovary or pelvis in 15% to 50% of cases,13,14 leading researchers to propose that endometriosis is a precursor of these tumors. In contrast, a high-grade serous carcinoma is rarely associated with ovarian endometriosis.

A recent clinical study using serial transvaginal ultrasonography has demonstrated that approximately 50% of ovarian carcinomas develop from preexisting cystic lesions, whereas the remaining 50% develop in ovaries without apparent abnormality on ultrasound.15 The former group was composed mainly of mucinous, endometrioid, and clear cell carcinomas, and borderline tumors, whereas the latter group was composed almost exclusively of high-grade serous carcinomas.

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