51. Estrogens and Their Receptors in Prostate Cancer: Therapeutic Implications
- Author
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Pia Giovannelli, Gabriella Castoria, Marzia Di Donato, Giovanni Galasso, Erika Di Zazzo, Di Zazzo, Erika, Galasso, Giovanni, Giovannelli, Pia, DI DONATO, Marzia, and Castoria, Gabriella
- Subjects
0301 basic medicine ,Cancer Research ,Review ,lcsh:RC254-282 ,Management of prostate cancer ,estradiol receptors ,03 medical and health sciences ,Prostate cancer ,0302 clinical medicine ,estradiol ,Medicine ,Tumor growth ,Receptor ,new drugs ,business.industry ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,prostate cancer ,Androgen receptor ,030104 developmental biology ,Prostate cancer, castrate resistant prostate cancer, estradiol, estradiol receptors, new drugs ,Nuclear receptor ,Oncology ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,castrate resistant prostate cancer ,Signal transduction ,business - Abstract
A major challenge in clinical management of prostate cancer (PC) is to limit tumor growth and prevent metastatic spreading. Considerable efforts have been made to discover new compounds for PC therapy and recent years have seen promising progress in this field. Pharmacological approaches have been designed to achieve benefits in PC treatment and avoid the negative side effects resulting from administration of antagonists or agonists or new drugs. Nonetheless, the currently available therapies frequently induce resistance and PC progresses toward castration-resistant forms that can be caused by the androgen receptor reactivation and/or mutations, or derangement of signaling pathways. Preclinical and clinical findings have also shown that other nuclear receptors are frequently altered in PC. In this review, we focus on the role of estradiol/estradiol receptor (ER) axis, which controls PC growth and progression. Selective targeting of ER subtypes (α or β) may be an attractive way to limit the growth and spreading of prostatic cancer cells.
- Published
- 2018