Table 4.

Murine models of Pten mutations relating to ovarian tumorigenesis. Summary of Tg promoters used to drive Cre expression for Pten-floxed modification, ovarian and uterine phenotypes and other tissue-specific effects. All models targeted exon 5 of Pten

Promoter	Cre activity	Ovarian phenotype	Uterine phenotype	Other phenotypes
Amhr2 [27]	Few granulosa cells (early follicles) Ovarian surface epithelial cells Fallopian and uterine tissue	• 7 % Females had aggressive, anaplastic granulosa cell tumours with pulmonary metastases • Normal follicle development and growth, ovulation and formation and function of corpora lutea (CL)	• Devoid of uterine defects	• Mice failed to carry pregnancies to term or had small litters, suggested to be due to an extra-ovarian defect
Cyp19 [28]	Granulosa cells (antral and preovulatory follicles) Most luteal cells (CL)	• No ovarian tumour formation at 12 months of age • Increased ovulation and ovarian volume due to accumulation of CLs	• No reported uterine abnormality.	• Fertile and no extra-ovarian abnormalities detected
Pax [51]	Fallopian and uterine tissue	• High-grade serous ovarian cancer development	• Endometrial hyperplasia, dysplasia and carcinomas observed	• Some high-grade serous carcinomas originated in fallopian tube and metastasized to the ovary
AMH	Granulosa cells (small-large antral, some preovulatory follicles)	• No ovarian tumours at 12 months of age • No ovarian histological or functional anomalies	• Normal uterine phenotype	• No abnormalities detected
SOX2	Global heterozygous disruption	• No ovarian tumours • Increased ovarian volume due to accumulation of CLs	• Endometrial polyps, metaplasia, hyperplasia, dysplasia, adenoma, adenocarcinoma and choriocarcinoma	• Mammary, lymphatic, adrenal and pituitary abnormalities • Disrupted estrous cycling