cardiovascular studies. A decade ago, the FDA mandated safety labels of gonadotropin-releasing hormone (GnRH) agonists to include additional warnings about potential increased risks for diabetes and cardiovascular events, and advocated for physicians to closely
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Alice Dragomir, Nawar Touma, Jason Hu, Sylvie Perreault, and Armen G. Aprikian
Shinjini Ganguly, Zaeem Lone, Andrew Muskara, Anna Kondratova, Anthony Ghanem, Yoon-Mi Chung, Aimalie Hardaway, Monaben Patel, Elai Davicioni, Shilpa Gupta, Jay Ciezki, Jorge Garcia, Kevin Stephans, Rahul Tendulkar, Eric Klien, Nima Sharifi, and Omar Y. Mian
androgen directed therapy and nominates HSD3B1 genotype as a predictive biomarker of treatment response. An NCCN sponsored prospective validation cohort is currently accruing. Figure 1 Graphical Schema of HSD3B1’s role in GnRH agonist bypass and
Venkata K. Pokuri, Houman Nourkeyhani, Bodie Betsy, Laurie Herbst, Marcus Sikorski, Edward Spangenthal, Andrew Fabiano, and Saby George
difficult problems increasingly manageable, prompt recognition and the institution of adequate therapy are essential. Androgen deprivation therapy (ADT) with gonadotropin-releasing hormone (GnRH) agonists has remained the mainstay of prostate cancer
Philip J. Saylor and Matthew R. Smith
effective systemic treatment for prostate cancer. Whether accomplished through bilateral orchiectomies or treatment with a gonadotropin-releasing hormone (GnRH) agonist, ADT leads to severe hypogonadism. GnRH agonists, for instance, lower serum testosterone
therapy, eg, GnRH agonists, by converting circulating steroid precursors to androgens intracellularly. The rate limiting enzyme for this conversion is 3βHSD, which is stabilized by a common polymorphism (1245C). DHT biosynthesis downstreamof variant 3bHSD
Adrienne G. Waks and Ann H. Partridge
use of gonadotropin-releasing hormone (GnRH) agonists concurrent with chemotherapy. Use of GnRH agonists has been posited to improve the chances of ovarian recovery postchemotherapy through a variety of mechanisms, including decreasing ovarian and
Azeez Farooki
with various cancer therapies, including aromatase inhibitor (AI) therapy in postmenopausal women and AI therapy and gonadotropin-releasing hormone (GnRH) agonists in pre-menopausal women with breast cancer, bone marrow transplantation in patients with
Yan Hiu Athena Lee, Jiandong Zhou, Jeremy Man Ho Hui, Xuejin Liu, Teddy Tai Loy Lee, Kyle Hui, Jeffrey Shi Kai Chan, Abraham Ka Chung Wai, Wing Tak Wong, Tong Liu, Kenrick Ng, Sharen Lee, Edward Christopher Dee, Qingpeng Zhang, and Gary Tse
against all-cause mortality in younger patients. Subgroup Analysis by Use of ADT We analyzed the effect of ADT, including gonadotropin-releasing hormone (GnRH) agonists and antagonists, on all-cause mortality among metformin and sulfonylurea users
Peter F. Coccia, Alberto S. Pappo, Jessica Altman, Smita Bhatia, Scott C. Borinstein, Joseph Flynn, A. Lindsay Frazier, Suzanne George, Robert Goldsby, Robert Hayashi, Mary S. Huang, Rebecca H. Johnson, Lynda Kwon Beaupin, Michael P. Link, Kevin C. Oeffinger, Kathleen M. Orr, Damon Reed, Holly L. Spraker, Deborah A. Thomas, Margaret von Mehren, Daniel S. Wechsler, Kimberly F. Whelan, Brad Zebrack, Dorothy A. Shead, and Hema Sundar
investigational. Randomized trials that have evaluated the role of menstrual suppression with gonadotropin-releasing hormone (GnRH) agonists to preserve ovarian function during chemotherapy have provided conflicting reports. Three randomized trials showed that
Janice S. Kwon, Gary Pansegrau, Melica Nourmoussavi, Geoffrey L. Hammond, and Mark S. Carey
tamoxifen); or (3) OA accomplished by outpatient laparoscopic bilateral salpingo-oophorectomy (BSO), followed by 5 years of an AI. We did not model the use of gonadotropin-releasing hormone (GnRH) agonist as a method of OA/AI, because there is no evidence
