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Approximately 80% of human ovarian and endometrial cancers and 50% of breast cancers express GnRH and its receptor as part of an autocrine regulatory system. After binding of its ligand the tumor GnRH receptor couples to G-protein alphai and activates a variety of intracellular signaling mechanisms. (1) Through activation of a protein tyrosine phosphatase, autophosphorylation of growth factor receptors is reverted leading to an inhibition of mitogenic signaling and reduced cell proliferation. (2) Through activation of nuclear factor kappa B antiapoptotic mechanisms are induced protecting tumor cells from apoptosis induced, for example, by doxorubicin. (3) Through activation of the Jun kinase pathway AP-1 is induced, leading to cell cycle arrest in the G0/G1 phase. It seems reasonable to speculate that this system enables the tumor cell to reduce proliferation and to activate repair mechanisms while being protected simultaneously from apoptosis. Interestingly, GnRH antagonists show the same activity in this system as agonists, indicating that the dichotomy GnRH agonist-GnRH antagonist defined in the pituitary gonadotrope is not valid for the tumor GnRH system. Recently, a second type of GnRH receptor, specific for GnRH-II, has been identified in ovarian and endometrial cancers, which transmits significantly stronger antiproliferative effects than the GnRH-I receptor. GnRH antagonists have agonistic effects on this type II receptor. In animal models of human cancers, GnRH antagonists had stronger antitumor effects than GnRH agonists. Therefore, we performed a phase II clinical trial with the GnRH antagonist, cetrorelix (10 mg/day), in patients with ovarian or mullerian carcinoma refractory to platinum chemotherapy. Of 17 evaluable patients treated with cetrorelix, 3 obtained a partial remission (18%) which lasted for 2 to 6 months. Furthermore, 6 patients experienced disease stabilization (35%) for up to 1 year. In this very refractory patient population (median number of prior chemotherapies = 3) these results are quite remarkable when compared with palliative chemotherapy. In addition, cytotoxic GnRH analogs have been developed, where for example doxorubicin was covalently coupled to GnRH analogs. These compounds have superior antitumor effects in cancers expressing GnRH receptors as compared with native doxorubicin and allow for a targeted cytotoxic chemotherapy of gynecologic and breast cancers.
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of unknown ER status by reducing breast cancer recurrence and mortality. However, it is universally accepted that standard TAM dosages may be responsible for endometrial proliferation, hyperplasia, polyp formation, invasive carcinoma and uterine
The author and journal apologise for an error that occurred in the paper by Cong et al . in the September 2007 issue of Endocrine-Related Cancer 14 713–720 entitled ‘Human adiponectin inhibits cell growth and induces apoptosis in human
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endometrial adenocarcinoma cells . Endocrinology 44 2822 – 2828 . Hana V Murphy LJ 1994 Expression of insulin-like growth factors and their binding proteins in the estrogen responsive Ishikawa human endometrial cancer cell line . Endocrinology
Department of Medical and Clinical Genetics, Department of Cell and Molecular Biology, Department of Mathematical Statistics, Institute of Biomedicine, University of Gothenburg, Sahlgrenska Academy, SE 40530 Gothenburg, Sweden
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Department of Medical and Clinical Genetics, Department of Cell and Molecular Biology, Department of Mathematical Statistics, Institute of Biomedicine, University of Gothenburg, Sahlgrenska Academy, SE 40530 Gothenburg, Sweden
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Introduction Endometrial cancer is the most frequently diagnosed gynecological malignancy in the western world with an estimated incidence of 15–20 cases per 100 000 women per year ( Esteller et al . 1999 , Ryan et al . 2005 ). Endometrial
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Dame Roma Mitchell Cancer Research Laboratories School of Medicine, University of Adelaide, Adelaide, South Australia 5000, Australia
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Introduction In this issue, we bring together some fascinating aspects and novel insights into androgen signalling in endocrine cancers, focusing mostly on prostate cancer, but inclusive of breast, ovarian and endometrial cancers. One intriguing
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Department of Pathology, Helse Møre og Romsdal, Ålesund, Norway
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Stavanger-Gynekologene AS, Stavanger, Norway
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Dr. Med. Jan Baak AS, Tananger, Norway
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Department of Mathematics and Natural Sciences, University of Stavanger, Stavanger, Norway
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Introduction Endometrial cancer is currently the most frequent form of gynaecologic cancer in developed countries ( http://globocan.iarc.fr/Pages/fact_sheets_population.aspx , Accessed: 28 February 2018). Endometrial endometrioid cancer (EEC
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mutated or deleted in a wide range of human cancers, including uterine cancers ( Dahia 2000 ). Pten mutations are observed in 30–80% of type 1 endometrial carcinomas (EMCs) and in 20–70% of complex atypical hyperplasia, a premalignant stage of EMC
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for specific cancers in patients with diabetes mellitus showed increases in the relative risk of liver, pancreatic, colorectal, bladder, endometrial, and breast cancers, and non-Hodgkin's lymphoma ( Gallagher et al . 2010 b ). Insulin resistance
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Introduction Endometrial cancer (EC) is a frequent gynecological cancer. It is highly hormone dependent being promoted by estradiol (E 2 ) and inhibited by progesterone (P 4 ) ( Bender et al . 2011 ), while the role of androgens remains
