Table 1: Classification, origin, and mechanism of epithelial ovarian cancer.

Tumor type	Serous		Endometrioid	Clear cell	Mucinous
Tumor type	High-grade (Appendix 1)	Low-grade	Endometrioid	Clear cell	Mucinous
Incidence	34%	5%	16%	23%	12%
Tissue origin	Fallopian tube epithelium Ovarian surface epithelium	Fallopian tube epithelium Ovarian surface epithelium	Endometrial cells Ovarian surface epithelium	Endometrial cells Ovarian surface epithelium	Ovarian surface epithelium Brenner tumor (Appendix 4)
Precancerous lesion	STIC (Appendix 2)	Borderline malignant tumor (Appendix 3)	Atypical endometriosis	Atypical endometriosis	Borderline malignant tumor (Appendix 3)
Molecular biological abnormalities	p53 mutation BRCA1/2 mutation Chromosome instability	KRAS mutation BRAF mutation (BRCA1/2 mutation)	ERa high expression PI3KCA mutation CTNNB1 mutation ARID1A mutation BRCA1/2 mutation Microsatellite instability	HNF-1b high expression PI3KCA mutation PTEN mutation ARID1A mutation	KRAS mutation HER2 high expression
Sensitivity to chemotherapy	High	Middle	High	Low	Low
HBOC (Appendix 5)	+++	++	+	−	−
Type I/II	Type II	Type I
Incidence	Europe, USA > Asia	Europe, USA < Asia

STIC(Appendix 2): serous tubal intraepithelial carcinoma, Borderline malignant tumor(Appendix 3): Borderline ovarian tumors are abnormal cells that form in the tissue overlying the ovary. They are not cancerous and are generally treated surgically. Approximately 15 out of 100 ovarian tumors (15%) are borderline tumors. They are also described as atypical proliferative tumors and were previously known as tumors of low malignant potential. They are different from ovarian cancer because they do not grow into the supportive tissue of the ovary (the stroma). Their growth is gradual and more controlled manner than cancer cells. Borderline tumors generally affect women aged between 20 and 40 years. They are usually diagnosed at an early stage when abnormal cells are still within the ovary.