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. 2023 Feb 28;15(2):68–75. doi: 10.14740/jocmr4853

Table 1. Classification, Origin, and Mechanism of Epithelial Ovarian Cancer.

Tumor type Serous
Endometrioid Clear cell Mucinous
High grade Low grade
Incidence 34% 5% 16% 23% 12%
Tissue origin Fallopian tube epithelium Fallopian tube epithelium Endometrial cells Endometrial cells Ovarian surface epithelium
Ovarian surface epithelium Ovarian surface epithelium Ovarian surface epithelium Ovarian surface epithelium Brenner tumor
Precancerous lesion STIC [10] Borderline malignant tumor [11] Atypical endometriosis [12] Atypical endometriosis Borderline malignant tumor [11]
Molecular biological abnormalities p53 mutation KRAS mutation ERa high expression HNF-1β high expression KRAS mutation
BRCA1/2 mutation BRAF mutation PI3KCA mutation PI3KCA mutation HER2 high expression
Chromosome instability BRCA1/2 mutation CTNNB1 mutation PTEN mutation
ARID1A mutation ARID1A mutation
BRCA1/2 mutation
Microsatellite instability
Sensitivity to chemotherapy High Middle High Low Low
HBOC [13, 14] +++ ++ + - -
RRSO [13, 14] Recommend - - - -
Type I/II Type II Type I
Incidence Europe, USA > Asia Europe, USA < Asia

Borderline malignant tumors are abnormal cells that form in the tissue covering the ovary. They are not cancerous and are generally cured with surgery. Approximately 15 out of 100 ovarian tumors (15-20%) are borderline tumors [11]. They are also described as atypical proliferative tumors and were previously called tumors with low malignant potential [11]. They are different from ovarian cancer because they do not grow into the supportive tissue of the ovary (the stroma). They slowly grow and in a more controlled way than cancer cells. Borderline tumors generally affect women aged between 20 and 40 years. They are usually diagnosed at an early stage when the abnormal cells are still within the ovary. Ovarian atypical endometriosis is a premalignant lesion, and its potential to progress to endometriosis-associated ovarian cancer highlights its significance [12]. In BRCA1/2-associated hereditary breast and ovarian cancer (HBOC), female and male breast and ovarian cancers (including fallopian tube and primary peritoneal cancers) can occur [13]. To a lesser extent, the development of other cancers, such as prostate and pancreatic cancers, is allowed [13]. Melanoma primarily affects individuals with BRCA2 pathogenic variants. The risk of developing associated cancers depends on whether HBOC is caused by BRCA1/2 pathogenic variants. Pathogenic germline variants underlie up to 20% of ovarian carcinoma (OC) cases and are associated with varying degrees of OC risk [14]. For pathogenic mutations in high-penetrance genes, such as BRCA1/2, the role of risk-reducing bilateral salpingo-oophorectomy (RRSO) in cancer prevention is well established, thus improving the mortality rate [14]. STIC: serous tubal intraepithelial carcinoma; HNF-1β: hepatocyte nuclear factor-1 beta; HGSC: high-grade serous carcinoma; ER: estrogen receptor.