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Andrew V. Schally - One of the best experts on this subject based on the ideXlab platform.
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Direct growth inhibition of human endometrial cancer cells by the gonadotropin-releasing Hormone Antagonist SB-75: Role of apoptosis
American Journal of Obstetrics and Gynecology, 2013Co-Authors: D. Kleinman, Amos Douvdevani, J Levy, Andrew V. Schally, Yoav SharoniAbstract:Objective: Our objective was to study the direct action of the gonadotropin-releasing Hormone Antagonist SB-75 and the agonist buserelin on the proliferation of endometrial cancer cells. Study Design: Two human endometrial cell lines that differ in histologic subtype and estrogen receptor content were treated with gonadotropin-releasing Hormone analog. We measured the number of viable cells, cell cycle parameters, and apoptotic processes. Results: Growth of the Ishikawa cells was inhibited by SB-75 in a dose-dependent manner. 17β-Estradiol partially abolished the inhibitory effect of SB-75. The growth of the HEC-1A cells was not affected by the Antagonist. Neither endometrial cancer cell line showed significant sensitivity to the agonist buserelin. Tenfold concentration of the gonadotropin-releasing Hormone agonist did not abolish the inhibitory effect of the Antagonist on cell growth. The growth inhibition was not associated with any change in cell cycle parameters but was associated with an induction of apoptosis. Conclusion: The gonadotropin-releasing Hormone Antagonist SB-75 directly inhibits the growth of some human endometrial cancer cells and thus may be suitable for the treatment of endometrial tumors.
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Combining Growth Hormone-Releasing Hormone Antagonist With Luteinizing Hormone-Releasing Hormone Antagonist Greatly Augments Benign Prostatic Hyperplasia Shrinkage
The Journal of urology, 2012Co-Authors: Ferenc G Rick, Luca Szalontay, Marta Zarandi, Norman L. Block, Andrew V. Schally, Mehrdad Nadji, Karoly Szepeshazi, Irving Vidaurre, Magdolna Kovacs, Zoltan RekasiAbstract:Purpose: Benign prostatic hyperplasia often affects aging men. Antagonists of the neuropeptide growth Hormone-releasing Hormone reduced prostate weight in an androgen induced benign prostatic hyperplasia model in rats. Luteinizing Hormone-releasing Hormone Antagonists also produce marked, protracted improvement in lower urinary tract symptoms, reduced prostate volume and an increased urinary peak flow rate in men with benign prostatic hyperplasia. We investigated the influence of a combination of Antagonists of growth Hormone-releasing Hormone and luteinizing Hormone-releasing Hormone on animal models of benign prostatic hyperplasia.Materials and Methods: We evaluated the effects of the growth Hormone-releasing Hormone Antagonist JMR-132, given at a dose of 40 μg daily, the luteinizing Hormone-releasing Hormone Antagonist cetrorelix, given at a dose of 0.625 mg/kg, and their combination on testosterone induced benign prostatic hyperplasia in adult male Wistar rats in vivo. Prostate tissue was examined bio...
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efficacy and safety of luteinizing Hormone releasing Hormone Antagonist cetrorelix in the treatment of symptomatic benign prostatic hyperplasia
The Journal of Clinical Endocrinology and Metabolism, 1998Co-Authors: Ana Maria Comaruschally, Maureen Colcolough, William Brannan, Andrew V. Schally, Manoj MongaAbstract:As the life expectancy for men increases, more cases of benign prostatic hyperplasia (BPH) will be expected. Symptomatic BPH causes morbidity and can lower the quality of life. We investigated whether short term administration of the LH-releasing Hormone Antagonist cetrorelix could provide an improved treatment for men with BPH. Thirteen patients with moderate to severe symptomatic BPH were treated with cetrorelix (5 mg, sc, twice daily for 2 days followed by 1 mg/day, sc, for 2 months). Patients were evaluated at baseline, during treatment, and up to 18 months after therapy. We determined the effects of cetrorelix on the International Prostate Symptom Score (IPSS), Quality of Life score, sexual function, prostate size, uroflowmetry, and hormonal levels. Treatment with cetrorelix produced a decline of 52.9% (P < 0.0001) in IPSS, a 46% improvement in the Quality of Life score (P < 0.001), a rapid reduction of 27% (P < 0.006) in prostatic volume, and an increase in peak urinary flow rates by 2.86 mL/s. Seru...
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treatment of uterine leiomyomas with luteinizing Hormone releasing Hormone Antagonist cetrorelix
Human Reproduction, 1997Co-Authors: David Gonzalezbarcena, Raquel Banuelos Alvarez, Elizabeth Pere Ochoa, Imelda Cardenas Cornejo, Ana Maria Comaruschally, Juergen Engel, Thomas Reissmann, Andrew V. Schally, Hilde RiethmullerwinzenAbstract:The efficacy of the luteinizing Hormone-releasing Hormone Antagonist Cetrorelix (SB-75) in the medical management of uterine leiomyomas (fibromas) was evaluated. Cetrorelix was administered to 18 pre-menopausal women with myomas with a mean age of 33.3 years, who had been candidates for hysterectomy. The initial dose of Cetrorelix was 5 mg twice daily s.c. for the first 2 days and thereafter 0.8 mg was given twice daily s.c. for at least 3 months. The mean duration of the treatment was 4.4 months. Before the therapy with Cetrorelix, the mean uterine volume, measured by ultrasonography, was 395.4 ± 69.2 ml (range 89-1166). Sixteen patients showed a progressive reduction in uterine volume from 410.4 ± 77.1 to a mean of 230.8 ± 52.6 ml at 3 months. All patients became amenorrhoeic and had hot flushes. After treatment with Cetrorelix, a surgical myomectomy was performed in 12 women. One of the patients subjected to myomectomy after therapy with Cetrorelix became pregnant. These patients have been followed for up to 25 months and only in one case has the uterine volume increased after therapy. Three patients had good responses to therapy with Cetrorelix and it was decided to follow them only by observation. One patient became pregnant 2 months later. In the other patient, the uterine volume remained unchanged for the duration of the follow-up of 2 years and the third patient showed an increase after 21 months. In three patients, it was necessary to perform total hysterectomy. In 14 patients, serum concentrations of luteinizing Hormone, follicle stimulating Hormone and oestradiol decreased after the administration of the first dose of Cetrorelix and continued at subnormal values throughout therapy. In 15 patients who were not subjected to total hysterectomy, menstrual function returned at 1 month after cessation of treatment. Overall results support the use of Cetrorelix for the management of uterine leiomyomas.
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Direct growth inhibition of human endometrial cancer cells by the gonadotropin‐releasing Hormone Antagonist SB‐75: Role of apoptosis
International Journal of Gynecology & Obstetrics, 1994Co-Authors: D. Kleinman, Amos Douvdevani, J Levy, Andrew V. Schally, Yoav SharoniAbstract:OBJECTIVE: Our objective was to study the direct action of the gonadotropin-releasing Hormone Antagonist 88-75 and the agonist buserelin on the proliferation of endometrial cancer cells. STUDY DESIGN: Two human endometrial cell lines that differ in histologic subtype and estrogen receptor content were treated with gonadotropin-releasing Hormone analog. We measured the number of viable cells, cell cycle parameters, and apoptotic processes. RESULTS: Growth of the Ishikawa cells was inhibited by 88-75 in a dose-dependent manner. 17j3-Estradiol partially abolished the inhibitory effect of 88-75. The growth of the HEC-1A cells was not affected by the Antagonist. Neither endometrial cancer cell line showed significant sensitivity to the agonist buserelin. Tenfold concentration of the gonadotropin-releasing Hormone agonist did not abolish the inhibitory effect of the Antagonist on cell growth. The growth inhibition was not associated with any change in cell cycle parameters but was associated with an induction of apoptosis. CONCLUSION: The gonadotropin-releasing Hormone Antagonist 88-75 directly inhibits the growth of some human endometrial cancer cells and thus may be suitable for the treatment of endometrial tumors. (AM J OSSTET GYNECOl 1994;170:96-102.)
D. B. Dunger - One of the best experts on this subject based on the ideXlab platform.
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The effects of a specific growth Hormone Antagonist on overnight insulin requirements and insulin sensitivity in young adults with Type 1 diabetes mellitus
Diabetologia, 2003Co-Authors: R. M. Williams, R. Amin, F. Shojaee-moradie, A. M. Umpleby, C. L. Acerini, D. B. DungerAbstract:Aims/hypothesis Growth Hormone hypersecretion in Type 1 diabetes could exacerbate insulin resistance and contribute to declining glycaemic control. Our aim was to determine the effects of specific growth Hormone blockade on insulin sensitivity and lipolysis in young adults with Type 1 diabetes. Methods We studied the effects of two doses of a specific growth Hormone Antagonist (B2036-PEG; Somavert, Pharmacia Corporation, Milton Keynes, UK) on insulin sensitivity in seven young adults (17–22 yrs, 3M) with Type 1 diabetes. Subjects recieved 5 and 10 mg B2036-PEG, in random order for 3 weeks, with a 3-week washout. At baseline and following each treatment block, an overnight (03:00 to 08:00 h) insulin infusion for euglycaemia (5 mmol/l), followed by two-step hyperinsulinaemic euglycaemic clamp, using [6,6 ^2H_2] glucose and ^2H_5 glycerol to measure glucose and glycerol turnover was performed. Results Compared to baseline, overnight insulin requirements decreased with both doses: (means±SEM) 0.34±0.02 mU/Kg/min vs 0.25±0.01 (5 mg) ( p =0.04), and 0.24±0.01 (10 mg) ( p =0.004). IGF-I (ng/ml) decreased following 10 mg [223.5±23.9 vs 154.6±28.1 ( p =0.005], but not 5 mg. Mean overnight non esterified fatty acid concentrations (mmol/l) decreased with 10 mg [0.51±0.04 vs 0.38±0.04 ( p =0.03)], as did β-hydroxybutyrate (mmol/l); [0.31±0.04 vs 0.15±0.02 ( p =0.004)]. Glycerol production rate, an index of lipolysis, was lower following 10 mg ( p =0.04), but insulin sensitivity during the clamp did not change with either dose. Conclusion/interpretation Treatment with both doses of B2036-PEG reduced overnight insulin requirements. The 10 mg dose suppressed lipolysis and reduced IGF-I. Failure to show enhanced insulin sensitivity during the clamp with the 10 mg dose could reflect opposing actions of growth Hormone and IGF-I.
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The effects of a specific growth Hormone Antagonist on overnight insulin requirements and insulin sensitivity in young adults with Type 1 diabetes mellitus
Diabetologia, 2003Co-Authors: R. M. Williams, R. Amin, F. Shojaee-moradie, A. M. Umpleby, C. L. Acerini, D. B. DungerAbstract:Aims/hypothesis Growth Hormone hypersecretion in Type 1 diabetes could exacerbate insulin resistance and contribute to declining glycaemic control. Our aim was to determine the effects of specific growth Hormone blockade on insulin sensitivity and lipolysis in young adults with Type 1 diabetes. Methods We studied the effects of two doses of a specific growth Hormone Antagonist (B2036-PEG; Somavert, Pharmacia Corporation, Milton Keynes, UK) on insulin sensitivity in seven young adults (17–22 yrs, 3M) with Type 1 diabetes. Subjects recieved 5 and 10 mg B2036-PEG, in random order for 3 weeks, with a 3-week washout. At baseline and following each treatment block, an overnight (03:00 to 08:00 h) insulin infusion for euglycaemia (5 mmol/l), followed by two-step hyperinsulinaemic euglycaemic clamp, using [6,6 ^2H_2] glucose and ^2H_5 glycerol to measure glucose and glycerol turnover was performed. Results Compared to baseline, overnight insulin requirements decreased with both doses: (means±SEM) 0.34±0.02 mU/Kg/min vs 0.25±0.01 (5 mg) ( p =0.04), and 0.24±0.01 (10 mg) ( p =0.004). IGF-I (ng/ml) decreased following 10 mg [223.5±23.9 vs 154.6±28.1 ( p =0.005], but not 5 mg. Mean overnight non esterified fatty acid concentrations (mmol/l) decreased with 10 mg [0.51±0.04 vs 0.38±0.04 ( p =0.03)], as did β-hydroxybutyrate (mmol/l); [0.31±0.04 vs 0.15±0.02 ( p =0.004)]. Glycerol production rate, an index of lipolysis, was lower following 10 mg ( p =0.04), but insulin sensitivity during the clamp did not change with either dose. Conclusion/interpretation Treatment with both doses of B2036-PEG reduced overnight insulin requirements. The 10 mg dose suppressed lipolysis and reduced IGF-I. Failure to show enhanced insulin sensitivity during the clamp with the 10 mg dose could reflect opposing actions of growth Hormone and IGF-I.
R. M. Williams - One of the best experts on this subject based on the ideXlab platform.
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The effects of a specific growth Hormone Antagonist on overnight insulin requirements and insulin sensitivity in young adults with Type 1 diabetes mellitus
Diabetologia, 2003Co-Authors: R. M. Williams, R. Amin, F. Shojaee-moradie, A. M. Umpleby, C. L. Acerini, D. B. DungerAbstract:Aims/hypothesis Growth Hormone hypersecretion in Type 1 diabetes could exacerbate insulin resistance and contribute to declining glycaemic control. Our aim was to determine the effects of specific growth Hormone blockade on insulin sensitivity and lipolysis in young adults with Type 1 diabetes. Methods We studied the effects of two doses of a specific growth Hormone Antagonist (B2036-PEG; Somavert, Pharmacia Corporation, Milton Keynes, UK) on insulin sensitivity in seven young adults (17–22 yrs, 3M) with Type 1 diabetes. Subjects recieved 5 and 10 mg B2036-PEG, in random order for 3 weeks, with a 3-week washout. At baseline and following each treatment block, an overnight (03:00 to 08:00 h) insulin infusion for euglycaemia (5 mmol/l), followed by two-step hyperinsulinaemic euglycaemic clamp, using [6,6 ^2H_2] glucose and ^2H_5 glycerol to measure glucose and glycerol turnover was performed. Results Compared to baseline, overnight insulin requirements decreased with both doses: (means±SEM) 0.34±0.02 mU/Kg/min vs 0.25±0.01 (5 mg) ( p =0.04), and 0.24±0.01 (10 mg) ( p =0.004). IGF-I (ng/ml) decreased following 10 mg [223.5±23.9 vs 154.6±28.1 ( p =0.005], but not 5 mg. Mean overnight non esterified fatty acid concentrations (mmol/l) decreased with 10 mg [0.51±0.04 vs 0.38±0.04 ( p =0.03)], as did β-hydroxybutyrate (mmol/l); [0.31±0.04 vs 0.15±0.02 ( p =0.004)]. Glycerol production rate, an index of lipolysis, was lower following 10 mg ( p =0.04), but insulin sensitivity during the clamp did not change with either dose. Conclusion/interpretation Treatment with both doses of B2036-PEG reduced overnight insulin requirements. The 10 mg dose suppressed lipolysis and reduced IGF-I. Failure to show enhanced insulin sensitivity during the clamp with the 10 mg dose could reflect opposing actions of growth Hormone and IGF-I.
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The effects of a specific growth Hormone Antagonist on overnight insulin requirements and insulin sensitivity in young adults with Type 1 diabetes mellitus
Diabetologia, 2003Co-Authors: R. M. Williams, R. Amin, F. Shojaee-moradie, A. M. Umpleby, C. L. Acerini, D. B. DungerAbstract:Aims/hypothesis Growth Hormone hypersecretion in Type 1 diabetes could exacerbate insulin resistance and contribute to declining glycaemic control. Our aim was to determine the effects of specific growth Hormone blockade on insulin sensitivity and lipolysis in young adults with Type 1 diabetes. Methods We studied the effects of two doses of a specific growth Hormone Antagonist (B2036-PEG; Somavert, Pharmacia Corporation, Milton Keynes, UK) on insulin sensitivity in seven young adults (17–22 yrs, 3M) with Type 1 diabetes. Subjects recieved 5 and 10 mg B2036-PEG, in random order for 3 weeks, with a 3-week washout. At baseline and following each treatment block, an overnight (03:00 to 08:00 h) insulin infusion for euglycaemia (5 mmol/l), followed by two-step hyperinsulinaemic euglycaemic clamp, using [6,6 ^2H_2] glucose and ^2H_5 glycerol to measure glucose and glycerol turnover was performed. Results Compared to baseline, overnight insulin requirements decreased with both doses: (means±SEM) 0.34±0.02 mU/Kg/min vs 0.25±0.01 (5 mg) ( p =0.04), and 0.24±0.01 (10 mg) ( p =0.004). IGF-I (ng/ml) decreased following 10 mg [223.5±23.9 vs 154.6±28.1 ( p =0.005], but not 5 mg. Mean overnight non esterified fatty acid concentrations (mmol/l) decreased with 10 mg [0.51±0.04 vs 0.38±0.04 ( p =0.03)], as did β-hydroxybutyrate (mmol/l); [0.31±0.04 vs 0.15±0.02 ( p =0.004)]. Glycerol production rate, an index of lipolysis, was lower following 10 mg ( p =0.04), but insulin sensitivity during the clamp did not change with either dose. Conclusion/interpretation Treatment with both doses of B2036-PEG reduced overnight insulin requirements. The 10 mg dose suppressed lipolysis and reduced IGF-I. Failure to show enhanced insulin sensitivity during the clamp with the 10 mg dose could reflect opposing actions of growth Hormone and IGF-I.
Thomas S Scanlan - One of the best experts on this subject based on the ideXlab platform.
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rational design and synthesis of a novel thyroid Hormone Antagonist that blocks coactivator recruitment
Journal of Medicinal Chemistry, 2002Co-Authors: Ngoc Ha Nguyen, James W Apriletti, Suzana Cunha T Lima, Paul Webb, John D Baxter, Thomas S ScanlanAbstract:Recent efforts have focused on the design and synthesis of thyroid Hormone (T3) Antagonists as potential therapeutic agents and chemical probes to understand Hormone-signaling pathways. We previously reported the development of novel first-generation T3 Antagonists DIBRT, HY-4, and GC-14 using the “extension hypothesis” as a general guideline in Hormone Antagonist design.1-3 These compounds contain extensions at the 5‘-position (DIBRT, GC-14) of the outer thyronine ring or from the bridging carbon (HY-4). All of these compounds have only a modest affinity and potency for the thyroid Hormone receptor (TR) that limits studies of their Antagonistic actions. Here, we report the design and synthesis of a novel series of 5‘-phenylethynyl derivatives sharing the GC-1 halogen-free thyronine scaffold.4 One compound (NH-3) is a T3 Antagonist with negligible TR agonist activity and improved TR binding affinity and potency that allow for further characterization of its observed activity. One mechanism for antagonism ...
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rational design and synthesis of a novel thyroid Hormone Antagonist that blocks coactivator recruitment
Journal of Medicinal Chemistry, 2002Co-Authors: Ngoc Ha Nguyen, James W Apriletti, Suzana Cunha T Lima, Paul Webb, John D Baxter, Thomas S ScanlanAbstract:Recent efforts have focused on the design and synthesis of thyroid Hormone (T(3)) Antagonists as potential therapeutic agents and chemical probes to understand Hormone-signaling pathways. We previously reported the development of novel first-generation T(3) Antagonists DIBRT, HY-4, and GC-14 using the "extension hypothesis" as a general guideline in Hormone Antagonist design.(1-3) These compounds contain extensions at the 5'-position (DIBRT, GC-14) of the outer thyronine ring or from the bridging carbon (HY-4). All of these compounds have only a modest affinity and potency for the thyroid Hormone receptor (TR) that limits studies of their Antagonistic actions. Here, we report the design and synthesis of a novel series of 5'-phenylethynyl derivatives sharing the GC-1 halogen-free thyronine scaffold.(4) One compound (NH-3) is a T(3) Antagonist with negligible TR agonist activity and improved TR binding affinity and potency that allow for further characterization of its observed activity. One mechanism for antagonism appears to be the ability of NH-3 to block TR-coactivator interactions. NH-3 will be a useful pharmacological tool for further study of T(3) signaling and TR function.
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A Thyroid Hormone Antagonist That Inhibits Thyroid Hormone Action in Vivo
Journal of Biological Chemistry, 2002Co-Authors: Ngoc Ha Nguyen, Ha Yung Yang, Thomas S. Scanlan, Ngoc Ha Nguyen, Thomas S Scanlan, J. David FurlowAbstract:Abstract We have characterized the newly developed thyroid Hormone Antagonist NH-3 in both cell culture and in vivomodel systems. NH-3 binds Xenopus laevisthyroid Hormone receptors directly in vitro and induces a conformation distinct from agonist-bound receptors. Transcriptional activation of a thyroid Hormone response element-containing reporter gene is strongly inhibited by NH-3 in a dose-dependent manner. In addition, NH-3 prevents X. laevis thyroid Hormone receptors from binding to the p160 family of co-activators GRIP-1 and SRC-1 in a two-hybrid assay. To assess the potency of the compound in vivo, we used induced and spontaneous X. laevis tadpole metamorphosis, a thyroid Hormone-dependent developmental process. NH-3 inhibits thyroid Hormone-induced morphological changes in a dose-dependent manner and inhibits the up-regulation of endogenous thyroid Hormone-responsive genes. Spontaneous metamorphosis is efficiently and reversibly arrested by NH-3 with at least the same effectiveness as the thyroid Hormone synthesis inhibitor methimazole. Therefore, NH-3 is the first thyroid Hormone Antagonist to demonstrate potent inhibition of thyroid Hormone action in both cell culture- and whole animal-based assays.
Yoav Sharoni - One of the best experts on this subject based on the ideXlab platform.
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Direct growth inhibition of human endometrial cancer cells by the gonadotropin-releasing Hormone Antagonist SB-75: Role of apoptosis
American Journal of Obstetrics and Gynecology, 2013Co-Authors: D. Kleinman, Amos Douvdevani, J Levy, Andrew V. Schally, Yoav SharoniAbstract:Objective: Our objective was to study the direct action of the gonadotropin-releasing Hormone Antagonist SB-75 and the agonist buserelin on the proliferation of endometrial cancer cells. Study Design: Two human endometrial cell lines that differ in histologic subtype and estrogen receptor content were treated with gonadotropin-releasing Hormone analog. We measured the number of viable cells, cell cycle parameters, and apoptotic processes. Results: Growth of the Ishikawa cells was inhibited by SB-75 in a dose-dependent manner. 17β-Estradiol partially abolished the inhibitory effect of SB-75. The growth of the HEC-1A cells was not affected by the Antagonist. Neither endometrial cancer cell line showed significant sensitivity to the agonist buserelin. Tenfold concentration of the gonadotropin-releasing Hormone agonist did not abolish the inhibitory effect of the Antagonist on cell growth. The growth inhibition was not associated with any change in cell cycle parameters but was associated with an induction of apoptosis. Conclusion: The gonadotropin-releasing Hormone Antagonist SB-75 directly inhibits the growth of some human endometrial cancer cells and thus may be suitable for the treatment of endometrial tumors.
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Direct growth inhibition of human endometrial cancer cells by the gonadotropin‐releasing Hormone Antagonist SB‐75: Role of apoptosis
International Journal of Gynecology & Obstetrics, 1994Co-Authors: D. Kleinman, Amos Douvdevani, J Levy, Andrew V. Schally, Yoav SharoniAbstract:OBJECTIVE: Our objective was to study the direct action of the gonadotropin-releasing Hormone Antagonist 88-75 and the agonist buserelin on the proliferation of endometrial cancer cells. STUDY DESIGN: Two human endometrial cell lines that differ in histologic subtype and estrogen receptor content were treated with gonadotropin-releasing Hormone analog. We measured the number of viable cells, cell cycle parameters, and apoptotic processes. RESULTS: Growth of the Ishikawa cells was inhibited by 88-75 in a dose-dependent manner. 17j3-Estradiol partially abolished the inhibitory effect of 88-75. The growth of the HEC-1A cells was not affected by the Antagonist. Neither endometrial cancer cell line showed significant sensitivity to the agonist buserelin. Tenfold concentration of the gonadotropin-releasing Hormone agonist did not abolish the inhibitory effect of the Antagonist on cell growth. The growth inhibition was not associated with any change in cell cycle parameters but was associated with an induction of apoptosis. CONCLUSION: The gonadotropin-releasing Hormone Antagonist 88-75 directly inhibits the growth of some human endometrial cancer cells and thus may be suitable for the treatment of endometrial tumors. (AM J OSSTET GYNECOl 1994;170:96-102.)
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Direct growth inhibition of human endometrial cancer cells by the gonadotropin-releasing Hormone Antagonist SB-75: role of apoptosis.
American journal of obstetrics and gynecology, 1994Co-Authors: D. Kleinman, Amos Douvdevani, J Levy, Andrew V. Schally, Yoav SharoniAbstract:Our objective was to study the direct action of the gonadotropin-releasing Hormone Antagonist SB-75 and the agonist buserelin on the proliferation of endometrial cancer cells. Two human endometrial cell lines that differ in histologic subtype and estrogen receptor content were treated with gonadotropin-releasing Hormone analog. We measured the number of viable cells, cell cycle parameters, and apoptotic processes. Growth of the Ishikawa cells was inhibited by SB-75 in a dose-dependent manner. 17 beta-Estradiol partially abolished the inhibitory effect of SB-75. The growth of the HEC-1A cells was not affected by the Antagonist. Neither endometrial cancer cell line showed significant sensitivity to the agonist buserelin. Tenfold concentration of the gonadotropin-releasing Hormone agonist did not abolish the inhibitory effect of the Antagonist on cell growth. The growth inhibition was not associated with any change in cell cycle parameters but was associated with an induction of apoptosis. The gonadotropin-releasing Hormone Antagonist SB-75 directly inhibits the growth of some human endometrial cancer cells and thus may be suitable for the treatment of endometrial tumors.