Skip to main content
. 2019 Nov 25;9(2):421–431. doi: 10.1002/cam4.2725

Table 1.

Identification of driver gene mutations required for serous carcinogenesis in mouse model or in vitro carcinogenesis model

Genotype Knockout mouse model (Ref. 32)
Number of mice STIC Ovarian metastasis Peritoneal metastasis
BRCA1−/−, TP53MT, PTEN−/− 4 4/4 (100%) 1/4 (25%) 1/4 (25%)
BRCA1+ /−, TP53MT, PTEN−/− 12 10/12 (83%) 6/12 (50%) 8/12 (67%)
BRCA2−/−, TP53MT, PTEN−/− 12 9/12 (75%) 9/12 (75%) 8/12 (67%)
BRCA2+ /−, TP53MT, PTEN−/− 3 3/3 (100%) 3/3 (100%) 2/3 (67%)
TP53−/−, PTEN−/− 6 4/6 (67%) 0/6 (0%) 0/6 (0%)
BRCA2−/−, TP53−/− 11 11/11 (100%) NR 3/11 (27%)
Trangene Transgenic mouse model (Ref. 39)
Number of mice p53 signature STIC Invasive adenocarcinoma
TAg 34 34/34 (100%) 34/34 (100%) 19/34 (56%)
Introduced genetic factors In vitro carcinogenesis model (Ref. 40)
Number of mice Conlony formaiton on soft agar Tumor formation (subcutaneous) Tumor formation (intraperitoneal)
DN‐p53 4 0 0 0
DN‐p53, KRAS MT 4 0 0 0
DN‐p53, c‐Myc 4 0 0 0
DN‐p53, CA‐AKT 4 + 0 0
DN‐p53, KRAS MT c‐Myc 4 + 4 4
DN‐p53, KRAS MT, CA‐AKT 4 + 4 4

Abbreviations: CA‐AKT, constitutively activated AKT; DN‐p53, dominant negative form of p53; MT, mutation; STIC, serous tubal intraepithelial carcinoma; TAg, SV40 T antigen.