Type II Tumors

Type II ovarian tumors are clinically high grade at presentation and include the morphologically defined entities such as high-grade serous carcinoma (moderately and poorly differentiated), malignant mixed mesodermal tumors (carcinosarcomas), and undifferentiated carcinomas (see Table 2-2). In addition, it is likely that some rare high-grade endometrioid and clear cell carcinoma should also be included in this group. Although malignant mixed mesodermal tumors were once thought to be mixed tumors composed of carcinoma and sarcoma, recent studies have demonstrated that they are monoclonal.16,17 These tumors are now accordingly regarded as high-grade carcinomas with metaplastic sarcomatous elements. Type II carcinomas have been proposed to develop de novo from the surface epithelium or inclusion cysts of the ovary6; they are rarely associated with morphologically recognizable precursor lesions. They evolve rapidly, metastasize early in their course, and are highly aggressive (Figs. 2-2 and 2-3). It is likely that the apparent de novo conven-

Figure 2-2. High-grade ovarian serous carcinoma involving the omentum.

High-grade serous carcinoma has a strong tendency to involve the omentum, forming a "caking" appearance. The omentum was bread-loafed to reveal the solid tumor mass.

Figure 2-2. High-grade ovarian serous carcinoma involving the omentum.

High-grade serous carcinoma has a strong tendency to involve the omentum, forming a "caking" appearance. The omentum was bread-loafed to reveal the solid tumor mass.

Figure 2-3. High-grade ovarian cancer cells obtained from ascites. Tumor cells in the peritoneal fluid form ball-like clusters.

tional high-grade serous carcinoma does develop in a stepwise manner, but precursor lesions have not yet been elucidated molecularly or morphologically. Presumably, this is because of rapid transit from inception as a microscopic carcinoma to a clinically diagnosed neoplasm. Thus, the window to detect the precursor lesions appears to be very small.

This dualistic model is the first step in an attempt to elucidate the molecular pathogenesis of ovarian carcinoma, but it should not be construed as implying that all ovarian carcinomas follow the proposed pathways of tumorigenesis. In fact, Dehari and colleagues18 have demonstrated that in rare cases, a high-grade serous carcinoma is associated with either an invasive low-grade carcinoma or a serous borderline tumor. Mutational analysis of KRAS and BRAF in both low-grade/borderline component and high-grade component from the same cases shows that both areas share the same mutations in all informative cases. This finding strongly indicates that both low-grade carcinoma/borderline tumors and high-grade carcinomas are genetically related and suggests that a subset of high-grade carcinomas may likely arise from a preexisting low-grade carcinoma or a borderline tumor.18

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