Endocrine signaling in ovarian surface epithelium and cancer

被引:61
作者
Leung, Peter C. K. [1 ]
Choi, Jung-Hye [1 ]
机构
[1] Univ British Columbia, Dept Obstet & Gynecol, Child & Family Res Inst, Vancouver, BC V6H 3V5, Canada
基金
加拿大健康研究院;
关键词
GnRH; gonadotrophin; hormonal carcinogenesis and signalling pathway; ovarian cancer; ovarian surface epithelium; steroid;
D O I
10.1093/humupd/dml002
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Ovarian cancer is the sixth most common cancer and the fifth leading cause of cancer-related death among women in developed countries. Greater than 85% of human ovarian cancer arises within the ovarian surface epithelium (OSE), with the remainder derived from granulosa cells or, rarely, stroma or germ cells. The pathophysiology of ovarian cancer is the least understood among all major human malignancies because of a poor understanding of the aetiological factors and mechanisms of ovarian cancer progression. There is increasing evidence suggesting that several key reproductive hormones, such as GnRH, gonadotrophins and sex steroids, regulate the growth of normal OSE and ovarian cancer cells. The objective of this review was to highlight the effects of these endocrine factors on ovarian cancer cell growth and to summarize the signalling mechanisms involved in normal human OSE and its neoplastic counterparts.
引用
收藏
页码:143 / 162
页数:20
相关论文
共 323 条
[81]   Hormone replacement therapy and the risk of epithelial ovarian carcinoma: A meta-analysis [J].
Garg, PP ;
Kerlikowske, K ;
Subak, L ;
Grady, D .
OBSTETRICS AND GYNECOLOGY, 1998, 92 (03) :472-479
[82]   KI67 ANTIGEN IMMUNOSTAINING (MIB-1 MONOCLONAL-ANTIBODY) IN SEROUS OVARIAN-TUMORS - INDEX OF PROLIFERATIVE ACTIVITY WITH PROGNOSTIC-SIGNIFICANCE [J].
GARZETTI, GG ;
CIAVATTINI, A ;
GOTERI, G ;
DENICTOLIS, M ;
STRAMAZZOTTI, D ;
LUCARINI, G ;
BIAGINI, G .
GYNECOLOGIC ONCOLOGY, 1995, 56 (02) :169-174
[83]   Sheep exhibit novel variations in the organization of the mammalian type II gonadotropin-releasing hormone receptor gene [J].
Gault, PM ;
Morgan, K ;
Pawson, AJ ;
Millar, RP ;
Lincoln, GA .
ENDOCRINOLOGY, 2004, 145 (05) :2362-2374
[84]  
Gayther SA, 1996, AM J HUM GENET, V58, P451
[85]   Etiology of ovarian cancer: a proposed mechanism [J].
Ghahremani, M ;
Foghi, A ;
Dorrington, JH .
MEDICAL HYPOTHESES, 1999, 52 (01) :23-26
[86]   Mapping and characterization of the functional domains responsible for the differential activity of the A and B isoforms of the human progesterone receptor [J].
Giangrande, PH ;
Pollio, G ;
McDonnell, DP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (52) :32889-32900
[87]   Multiple Ras effector pathways contribute to G1 cell cycle progression [J].
Gille, H ;
Downward, J .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (31) :22033-22040
[88]  
GODWIN AK, 1993, CANCER-AM CANCER SOC, V71, P530
[89]  
GOLDENBERG GJ, 1982, CANCER RES, V42, P5147
[90]   Follicle-stimulating hormone (FSH) stimulates phosphorylation and activation of protein kinase B (PKB/Akt) and serum and glucocorticoid-induced kinase (Sgk): Evidence for A kinase-independent signaling by FSH in granulosa cells [J].
Gonzalez-Robayna, IJ ;
Falender, AE ;
Ochsner, S ;
Firestone, GL ;
Richards, JS .
MOLECULAR ENDOCRINOLOGY, 2000, 14 (08) :1283-1300