By Farr Nezhat, MD
Ovarian cancer, the deadliest of all gynecologic cancers, has provided a significant challenge for us. We are encouraged by the fact that survival of other gynecologic cancers, such as breast and cervical cancer, have increased dramatically in recent years; however, we must lower the incidence and mortality of ovarian cancer, as it has remained unchanged in 50 years.
I am reminded daily of the lack of an accurate early detection test for the disease and effective prevention strategy.
A new paradigm for ovarian cancer pathogenesis presupposes two distinct types of ovarian epithelial carcinoma with different molecular aberrations and mutations: Type I and Type II carcinomas. Type I tumors include endometrioid, clear cell carcinoma, and low grade serous carcinoma and arise via defined sequence either from endometriosis or from Serous cystadenoma and borderline serous tumors. More frequent, type II carcinomas are usually high grade serous tumors, and they seem arise from the fimbriated end of the fallopian tube. Subsequently, high-grade serous carcinomas present usually at advanced stages as a consequence of the peritoneal seeding from the open ends of the fallopian tubes without detectable precursor presently. On the other hand careful clinical evaluation of premalignant conditions leading to Type I cancers (ie: endometriomas and Serous cystadenoma) offers a possibility of early intervention.
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