Somatostatin Analogs and Disease Control in Castration-resistant Prostate Cancer: Different Biological Behavior? Case Series and Review of the Literature. Issue 3 (May 2014)

• Record Type: Journal Article
• Authors: D'Angelillo, Rolando Maria; Greco, Carlo; Fiore, Michele; Ippolito, Edy; Trodella, Luca Eolo; Iurato, Aurelia; Molfese, Elisabetta; Ramella, Sara; Trodella, Lucio
• Is Part Of: Tumori. Volume 100:Issue 3(2014)
• Page Start: 249
• Page End: 253
• Publication Date: 2014-05
• Subjects: castration-resistant prostate cancer -- neuroendocrine differentiation -- androgen deprivation therapy -- somatostatin analogs; Cancer -- Periodicals; 616.994
• DOI: 10.1700/1578.17192
• Languages: English
• ISSNs: 0300-8916

Abstract

Aims and Background: Castration-resistant prostate cancer is a recent biological behavior where disease can elude androgen deprivation therapy (ADT). Several pathways have been described, including neuroendocrine dedifferentiation. Patients with neuroendocrine dedifferentiation show an increase in chromogranin A (CgA) along with a PSA increase. Our aim was to evaluate the response of patients with castration-resistant prostate cancer and high CgA serum levels after treatment with inhibitors of neuroendocrine cells (somatostatin analogs) in combination with ADT. Methods: From January 2009 to April 2011, 10 patients with castration-resistant prostate cancer and rising PSA levels along with a CgA increase were evaluated. The therapy was based on somatostatin analogs and LHRH anologs. Total PSA and CgA were measured every 2 months. Results: In 9 of the 10 patients, a reduction of the values of pre-treatment CgA was detected, while a reduction of PSA was found in 8 patients. No grade 2 or higher toxicity was recorded. Only 3 patients had grade 1 gastrointestinal toxicity. Time to progression was 13 months. Conclusion: Therapy with somatostatin analogs could increase the therapeutic window of ADT with a low toxicity profile in a subpopulation of patients with castration-resistant prostate cancer who experience a rise in CgA due to neuroendocrine regulation.