The p53 tumor suppressor gene is the most commonly mutated gene in human cancer (Fig. 2-5). In contrast to low-grade serous carcinoma in which mutations in p53 are rare, mutations in p53 are common in high-grade serous carcinomas. Many studies have shown that 50% to 80% of advanced stage high-grade serous carcinomas have mutant p53.24-28 It has also been reported that mutant p53 is present in 37% of stage I and II presumably high-grade serous carcinomas.29 Overexpression ofp53 and mutation of p53 were found in all early invasive high-grade serous carcinomas as well as in the adjacent dysplastic surface epithelium, in a study of very early microscopic stage I serous carcinomas in ovaries removed prophylactically from women who were BRCA heterozygotes.30 It is likely that inherited mutations in BRCA genes predispose the peritoneal surface epithelium, ovarian surface inclusion cysts, and epithelial cells of the fimbriae ends of fallopian tubes to neoplastic transformation through an increase in genetic instability. Thus, it is conceivable that conventional high-grade serous carcinoma in its very earliest stage resembles advanced-stage serous carcinoma at a molecular as well as a morphologic level. Similar to high-grade serous carcinoma, most malignant mixed mesodermal tumors (carcinosarcomas) also demonstrate p53 mutations.31-33 It has been reported that the same p53 mutations occur in the epithelial and mesenchymal components.31 Moreover, the fact that pure carcinomatous areas are often associated with sarcomatous components suggests a common derivation of both epithelial and mesenchymal components in these neoplasms.34 The finding that metastases from these tumors nearly always are composed exclusively of carcinoma has led investigators to suggest that malignant mixed mesodermal tumors are metaplastic carcinomas.
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