From: The hormonal composition of follicular fluid and its implications for ovarian cancer pathogenesis
Factor | Role in follicle development | Potential role in pathogenesis | Mouse knockout model effect |
---|---|---|---|
Estradiol | Follicle development (specifically mid-follicular to pre-ovulatory phases) [28, 29] | Direct proliferatory effect [32], free radical generation [32], epidemiological risk factor for breast and uterine cancers [30] | Failure to develop mature follicles [28] |
Progesterone | Progestin containing oral contraceptives decrease ovarian cancer risk [41] | Failure to ovulate [28] | |
Androgens | Stimulates early follicle development [28] | Unknown | Decrease in fertility, granulosa cell number [28] |
FSH | Stimulation of primordial follicles, dominant follicle selection [45] | Hormonal regulator of estrogen, progestrone, testosterone, FSH and its signaling pathways highly expressed in OVCAR cell lines [46, 51] | Failure to ovulate, failure of primordial follicles to mature [46] |
AMH | Inhibits primordial follicle growth [56]. | Promotes growth and differentiation [54], elevated in granulosa cell tumors [62]. Unlikely player in HGSOC as matched controls have no difference in serum AMH, no correlation to stage or prognosis [63] | Fertile but with shorter period of fertility [56] |
LH | Supports thecal steroidogenesis, induces ovulation and corpus luteum formation [64] | Promotes angiogenesis in EOC through PI3K/AKT-mTOR pathway, inhibits apoptosis and cisplatin mediated apoptosis in EOC [69, 70] | Atrophied ovaries, hypogonadism, malformed antral follicles, no corpus lutea [66] |