(A) Pathogenesis The etiology of ovarian malignancies is unknown. The classification of ovarian tumors is as follows: 1. germ cell tumors asexual cell tumors, endodermal sinus tumors, teratomas (mature – substantial, cystic; immature, unilamellar epithelial – ovarian mesenchymal, carcinoid, neuroectodermal, mixed), embryonal carcinomas, malignant mixed germ cell tumors, polyembryoma, choriocarcinoma, gonadoblastoma. 2. Non-germ cell tumors Epithelial (plasmacytosis, mucinous), gonadal-stromal (granular, supportive-mesenchymal, mixed). (2) Pathogenesis 1. The “constant ovulation” theory of carcinogenesis: Ovarian tumors have a high incidence in women with early menarche, late menopause, and no childbirth, and a reduced risk in women with more childbirths, breastfeeding, and oral contraceptive use. This “constant ovulation” theory of carcinogenesis suggests that ovulation causes damage to ovarian epithelial cells, and that repeated damage and repair processes promote carcinogenesis. Genetic factors: It is one of the more researched causes in recent years, and most cases are inherited by autosomal dominant. In the last decade, molecular genetic studies have made great progress. Narod et al. identified a specific gene for carcinoma susceptibility in patients with hereditary breast-ovarian malignancy (HBOC) syndrome on chromosome 17, now called BRCA1, and recently another susceptibility gene, BRCA1, has been identified on chromosome 13. Mutations in these two genes allow most epithelial ovarian malignancies to form genetically. There are three main types of hereditary ovarian malignancies: (1) High-risk patients: One is familial ovarian malignancy syndrome, such as a mother or sister with ovarian malignancy, who is a high-risk patient herself. (2) 50% risk: It is a breast-ovarian malignancy syndrome, in which the mother or sister has one or two types of cancer, and the risk of ovarian malignancy is 50%. (3) Those with a family history of cancer: the risk of developing ovarian malignancy, endometrial cancer, breast cancer and colorectal cancer may be increased. 2. Histological grading: undifferentiated cells accounting for 0%-25% of the histology determined by Broder are G1; undifferentiated cells accounting for 25%-50% are G2; undifferentiated cells >50% are G3.