Introduction

Ovarian cancer is the most lethal gynecologic malignancy, and carcinoma is the most common type of ovarian cancer. The pathogenesis of ovarian carcinoma is still unclear, and one of the difficulties in studying ovarian cancer is the lack of a comprehensive tumor progression model. 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 in the organs of the female reproductive tract.1-3 The tumors in each of the categories are further subdivided into three groups, benign, malignant, and intermediate (borderline tumor or low-malignant-potential) based on their clinical behavior. It has been well known that mucinous and endometrioid borderline tumors are often associated with invasive carcinomas, but serous borderline tumors (SBTs) are rarely associated with serous carcinomas.1 The latter observation, as well as recent molecular genetic studies showing a very different mutation frequency of p53 and KRAS/BRAF/ERBB2 in serous carcinoma compared with serous borderline tumors, has led most investigators to conclude that serous borderline tumors and serous carcinomas are biologically unrelated.4-8 The uncertainty about the nature of the borderline tumor groups, reflected by the ambiguous term "borderline," is a major shortcoming of the current classification. Based on a review of recent clinical, histopathologic, and molecular genetic findings, a research team has proposed a new carcinogenesis model that reconciles the relation of borderline tumors to invasive carcinoma.

10 Ways To Fight Off Cancer

10 Ways To Fight Off Cancer

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