Neuroendocrine differentiation in castration resistant prostate cancer. Nuclear medicine radiopharmaceuticals and imaging techniques: A narrative review

• Published in: Critical reviews in oncology/hematology 2019-06, Vol.138, p.29-37
• Main Authors: Usmani, Sharjeel, Orevi, Marina, Stefanelli, Antonella, Zaniboni, Alberto, Gofrit, Ofer Nathan, Bnà, Claudio, Illuminati, Sonia, Lojacono, Giulia, Noventa, Silvia, Savelli, Giordano
• Format: Article
• Language: English
• Subjects: Androgen deprivation therapy; Castration-resistant prostate cancer; Neuroendocrine differentiation; Positron Emission Tomography; Somatostatin analogs; Somatostatin receptors
• ISSN: 1040-8428; 1879-0461
• DOI: 10.1016/j.critrevonc.2019.03.005

[Display omitted] Androgen Deprivation Therapy (ADT) is the primary treatment for patients suffering from relapsing or advanced prostate cancer (PC). Hormone therapy generally guarantees adequate clinical control of the disease for some years, even in those patients affected by widespread skeletal and soft tissue metastases. Despite ADT, however, most patients treated with hormones eventually progress to castration-resistant prostate cancer (CRPC), for which there are no effective treatments. This clinical reality is an open challenge to the oncologist because of those neoplasms which elaborate neuroendocrine differentiation (NED). An online search of current and past literature on NED in CRPC was performed. Relevant articles dealing with the biological and pathological basis of NED, with nuclear medicine imaging in CRPC and somatostatin treatment in NED were analyzed. NED may arise in prostate cancer patients in the late stages of ADT. The onset of NED offers prognostic insight because it reflects a dramatic increase in the aggressive nature of the neoplasm. Several genetic, molecular, cytological and immunohistochemical markers are associated with this transformation. Among these, overexpression of somatostatin receptors, seen through Nuclear Medicine testing, is one of the most studied. Preliminary studies show that the overexpression of somatostatin receptors related to NED in CRPC may easily be studied in vivo with PET/CT. This finding offers a potentially useful objective for targeted therapy in CRPC. If the overexpression of SSTRs is shown to afflict a significant segment of patients with CRPC, this will open further study of possible therapeutic options based on this marker.