Natini Jinawath and Ie-Ming Shih
Ovarian carcinomas are heterogeneous and are primarily classified by cell type into serous, mucinous, endometrioid, clear cell, and Brenner (transitional) tumors corresponding to different types of epithelia. The tumors in each category are further subdivided into three groups—benign, malignant, and intermediate—based on their clinical behavior.
Recent molecular genetic studies provide the basis for a more comprehensive model of ovarian carcinogenesis, which proposes two main pathways of tumorigenesis, corresponding to the development of type I and type II tumors.
Type I tumors (low-grade serous carcinoma) develop in a stepwise manner from well-accepted precursors. They are slow-growing and often confined to the ovary at the time of diagnosis. Type II tumors are clinically high-grade at presentation (high-grade serous carcinoma). They evolve rapidly, metastasize early in their course, and are highly aggressive.
Type I tumors frequently exhibit BRAF/KRAS gene mutations and low cellular proliferation. They usually have a gradual increase in cervical intraepithelial neoplasia (CIN) and are associated with a relatively long 5-year survival rate (~55%).
Type II tumors have frequent p53 mutations, HLA-G expression, and high cellular proliferation. They also show high cervical intraepithelial neoplasia and have a relatively short 5-year survival rate (~30%).
Protein kinase inhibitors are a promising novel therapy for ovarian cancers especially in type II tumors. It is interesting to see whether BRAF inhibitors and other MEK inhibitors can prolong disease-free interval and overall survival in patients with advanced-stage of SBTs.
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