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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, Andrew V. Schally, J Levy, 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, Andrew V. Schally, J Levy, 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, Andrew V. Schally, J Levy, 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.
Basil C. Tarlatzis - One of the best experts on this subject based on the ideXlab platform.
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fixed versus flexible gonadotropin releasing Hormone Antagonist administration in in vitro fertilization a randomized controlled trial
Fertility and Sterility, 2011Co-Authors: Efstratios M Kolibianakis, Christos A Venetis, Lydia Kalogeropoulou, E G Papanikolaou, Basil C. TarlatzisAbstract:Objective To evaluate whether the incidence of luteinizing Hormone (LH) rise is reduced by using a flexible compared with a fixed day-6 protocol of GnRH Antagonist administration. Design Randomized controlled trial. Setting Tertiary university hospital. Patient(s) Patients undergoing in vitro fertilization (n = 146). Intervention(s) Ovarian stimulation was performed using recombinant FSH and GnRH Antagonists. GnRH Antagonist cetrorelix (0.25 mg/d) was started either on day 6 of stimulation (fixed group) or when LH was >10 IU/L, and/or a follicle with mean diameter >12 mm was present, and/or serum E 2 was >150 pg/mL. Patient monitoring was initiated on day 3 of stimulation. Main Outcome Measure(s) Incidence of LH rise. Result(s) No statistically significant difference was observed between the flexible and fixed groups regarding the incidence of LH rise, which was lower in the flexible group (11.0% vs. 15.1%, difference −4.1%, 95% confidence interval −15.4% to +7.1%). No LH surges were observed in any of the patients studied. Conclusion(s) Flexible Antagonist administration from day 3 onward does not appear to reduce the incidence of LH rises compared with fixed Antagonist administration on day 6 of stimulation.
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Gonadotropin-Releasing Hormone Antagonists: impact of IVF practice and potential non-assisted reproductive technology applications.
Current opinion in obstetrics & gynecology, 2003Co-Authors: Basil C. Tarlatzis, Helen BiliAbstract:PURPOSE OF REVIEW To provide the clinician with updated knowledge of the most recent findings on the clinical use of Gonadotropin-Releasing Hormone Antagonists. RECENT FINDINGS Gonadotropin-Releasing Hormone Antagonists, which have recently been introduced in clinical practice, cause an immediate suppression of gonadotropin secretion by competitive blocking of pituitary Gonadotropin-Releasing Hormone receptors. Thus, they are effective in preventing the premature luteinizing Hormone surges during ovarian stimulation for in-vitro fertilization and may improve the patient's response to lower doses of gonadotropins. Better patient acceptance, shorter treatment cycles and fewer follicles and oocytes are also reported. Data existing so far concerning the necessity of luteal phase support after the use of Gonadotropin-Releasing Hormone Antagonists show that it might not be mandatory when used in clomiphene citrate costimulated cycles or in intrauterine insemination cycles. The use of Gonadotropin-Releasing Hormone Antagonists seems to be safe for pregnant women and their offspring. All sex-Hormone-dependent disorders, currently treated with Gonadotropin-Releasing Hormone agonists, may in future be indications for a Gonadotropin-Releasing Hormone Antagonist, including endometriosis, leiomyoma, and breast cancer in women, benign prostatic hypertrophy and prostatic carcinoma in men, and central precocious puberty in children. The vast majority of the available clinical data up till now, however, are in assisted reproduction and prostate cancer. SUMMARY It is expected that the availability of Gonadotropin-Releasing Hormone Antagonist will lead to the use of 'softer' ovarian stimulation protocols, which will be shorter, cheaper and safer compared with the conventional protocols.
D. Kleinman - 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, Andrew V. Schally, J Levy, 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, Andrew V. Schally, J Levy, 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, Andrew V. Schally, J Levy, 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.
Chikara Ohyama - One of the best experts on this subject based on the ideXlab platform.
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Efficacy of a neoadjuvant Gonadotropin-Releasing Hormone Antagonist plus low-dose estramustine phosphate in high-risk prostate cancer: A single-center study.
Journal of Clinical Oncology, 2017Co-Authors: Kazuhisa Hagiwara, Takuya Koie, Hayato Yamamoto, Atsushi Imai, Shingo Hatakeyama, Takahiro Yoneyama, Yasuhiro Hashimoto, Yuki Tobisawa, Tohru Yoneyama, Chikara OhyamaAbstract:e542Background: The optimal treatment for high-risk prostate cancer (Pca) remains to be established. We previously reported favorable biochemical recurrence-free survival (BRFS) for high-risk Pca patients treated with neoadjuvant therapy comprising a luteinizing Hormone-releasing Hormone agonist plus low-dose estramustine (LHRH agonist + EMP) prior to radical prostatectomy (RP). In the present study, we evaluated the efficacy of neoadjuvant therapy comprising a Gonadotropin-Releasing Hormone Antagonist plus low-dose estramustine phosphate (GnRH Antagonist + EMP) in patients with high-risk Pca. Methods: Between September 2005 and March 2016, we identified 406 high-risk Pca patients of whom 136 received neoadjuvant GnRH Antagonist + EMP and 270 received LHRH agonist + EMP before RP. We retrospectively evaluated the clinical and pathological covariates between the two groups. The primary endpoint was the rate of pathological ≤ T2 status, and the secondary endpoint was BRFS. Results: The rates of pathological...
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Efficacy of a neoadjuvant Gonadotropin-Releasing Hormone Antagonist plus low-dose estramustine phosphate in high-risk prostate cancer: a single-center study
International urology and nephrology, 2017Co-Authors: Kazuhisa Hagiwara, Takuya Koie, Chikara Ohyama, Hayato Yamamoto, Atsushi Imai, Shingo Hatakeyama, Takahiro Yoneyama, Yasuhiro Hashimoto, Yuki Tobisawa, Tohru YoneyamaAbstract:Purpose The optimal treatment for high-risk prostate cancer (Pca) remains to be established. We previously reported favorable biochemical recurrence-free survival (BRFS) for high-risk Pca patients treated with neoadjuvant therapy comprising a luteinizing Hormone-releasing Hormone agonist plus low-dose estramustine (LHRH + EMP) prior to radical prostatectomy (RP). In the present study, we evaluated the efficacy of neoadjuvant therapy comprising a Gonadotropin-Releasing Hormone Antagonist plus low-dose estramustine phosphate (GnRH + EMP) in patients with high-risk Pca.
Keith Gordon - One of the best experts on this subject based on the ideXlab platform.
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Ongoing Pregnancy Rates with Daily Recombinant Follicle-Stimulating Hormone/Gonadotropin-Releasing Hormone Antagonist Protocol in a Large North American Cohort of In Vitro Fertilization/Intracytoplasmic Sperm Injection Patients by Day of Embryo Trans
Fertility and Sterility, 2010Co-Authors: A. Lifchez, Z.p. Nagy, H. Witjes, Bernadette Mannaerts, Keith Gordon, M. MahonyAbstract:Ongoing Pregnancy Rates with Daily Recombinant Follicle-Stimulating Hormone/Gonadotropin-Releasing Hormone Antagonist Protocol in a Large North American Cohort of In Vitro Fertilization/Intracytoplasmic Sperm Injection Patients by Day of Embryo Transfer. A. Lifchez, Z.P. Nagy, H. Witjes, B. Mannaerts, K. Gordon, M. Mahony. on behalf of the Engage investigators Fertility Centers of Illinois, SC, Chicago, Illinois; Reproductive Biology Associates, Atlanta, Georgia; Schering-Plough Research Institute, Schering-Plough, a Division of Merck & Co., Oss, The Netherlands; and Schering-Plough, a Division of Merck & Co., Kenilworth, New Jersey.
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New trends in combined use of Gonadotropin-Releasing Hormone Antagonists with gonadotropins or pulsatile Gonadotropin-Releasing Hormone in ovulation induction and assisted reproductive technologies.
Current opinion in obstetrics & gynecology, 1992Co-Authors: Keith Gordon, Douglas R. Danforth, Robert F. Williams, Gary D. HodgenAbstract:The use of Gonadotropin-Releasing Hormone agonists as adjunctive therapy with gonadotropins for ovulation induction in in vitro fertilization and other assisted reproductive technologies has become common clinical practice. With the recent advent of potent Gonadotropin-Releasing Hormone Antagonists free from the marked histamine-release effects that stymied earlier compounds, an attractive alternative method may be available. We have established the feasibility of combining Gonadotropin-Releasing Hormone Antagonist-induced inhibition of endogenous gonadotropins with exogenous gonadotropin therapy for ovulation induction in a nonhuman primate model. Here, the principal benefits to be gained from using the Gonadotropin-Releasing Hormone Antagonist rather than the Gonadotropin-Releasing Hormone agonist are the immediate inhibition of pituitary gonadotropin secretion without the "flare effect," which brings greater safety and convenience for patients and the medical team and saves time and money. We have also recently demonstrated the feasibility of combining Gonadotropin-Releasing Hormone Antagonist with pulsatile Gonadotropin-Releasing Hormone therapy for the controlled restoration of gonadotropin secretion and gonadal steroidogenesis culminating in apparently normal (singleton) ovulatory cycles. This is feasible only with Gonadotropin-Releasing Hormone Antagonists because, unlike Gonadotropin-Releasing Hormone agonists, they achieve control of the pituitary-ovarian axis without down regulation of the Gonadotropin-Releasing Hormone receptor system. This capacity to override Gonadotropin-Releasing Hormone Antagonist-induced suppression of pituitary-ovarian function may allow new treatment modalities to be employed for women who suffer from chronic hyperandrogenemia with polycystic ovarian disease.