Review Article

Recent Concepts of Ovarian Carcinogenesis: Type I and Type II

Table 1

Summary of clinicopathological features and molecular genetic alterations of two types of ovarian carcinoma.

Type I tumorsType II tumors

BehaviorIndolentAggressive
At the time of the diagnosisEarly stageAdvanced stage
Survival rate at 5 yearsAbout 55%About 30%
Histological type/Precursors
Endometrioid carcinoma/EndometriosisHigh grade serous/Probably de novo starting at the tubo-
Clear cell carcinoma/Endometriosisovarian surface epithelium; SCOUT→
Mucinous carcinoma/Mucinous Cystadenoma, EndometriosisP53 signature→STIL/TILT→STIC
Teratoma, Brenner Tumor, and MBTor ovarian hilum stem cell
Low grade serous carcinoma/Serous cystadenoma, AdenofibromaUndifferentiated carcinoma/?
Atypical proliferative serous tumor (SBT)Carcinosarcoma/?
Müllerian epithelial cyst
Transitional cell carcinoma/Brenner tumor
Gene expression profile
 Genetic instabilityNot very unstableVery unstable
 PTEN mutation15–20%Low
 HNF-1 beta
 overexpression
90%Low
 ARID1A mutation40–50%Not found
 CTNNB1 mutation30%Low
 PIK3CA20%Low
 Microsatellite
 instability
50%8–28%
 KRAS mutation30–65%Low
 BRAF mutation30–65%Low
 TP53 mutationLow50–80%
 HER2/neu
 overexpression
Low20–67%
 AKT overexpressionLow12–30%
 p16 inactivationLow15%
 HLA-G
 overexpression
Low61%
 APO E
 overexpression
12%66%
 BRCA 1/BRCA2
 mutation
LowHigh
 Ki67 proliferation
 index
10–15%50–75%