Abstract:

The histogenesis of ovarian cancer has been facing challenges both clinically and molecular-histologically. This is due to the fact that most so-called ovarian carcinomas are neither from ovaries nor from the cell types we once believed.  Recent recognition of precursor lesions in high grade papillary serous carcinoma (H-PSC), defined as serous tubal intraepithelial carcinoma (STIC) in fimbria, highlights H-PSC as a new area of interest in the study of early tumorigenesis of type II ovarian cancer. Identification of STIC prompts us to search for molecular changes responsible for the early carcinogenesis of H-PSC. We are in the beginning stages of characterizing several critical genetic alterations, including P53, BRCA1, HMGA2 and certain microRNAs. Meanwhile, identification of STIC may cause us to re-evaluate the histogenesis of other types of ovarian cancer and their precursor lesions. For example, the cell origin of type I ovarian cancer, including endometrioid, clear cell, mucinous and some low-grade serous carcinomas, is likely originated from ectopic endometrium (endometriosis), metaplasia or the fallopian tubes. Characterizing the cell origin as well as the molecularoncogenic and cellular alterations in a stepwise tumor progression will greatly impact our understanding of the heterogeneity of these diseases and lead to potential targets for early detection, prevention and therapeutic modalities for this deadly disease. 

Key words: Ovary； Carcinoma in situ； Histogenesis； Origin