Neuroendocrine tumors of the prostate

Abstract

Neuroendocrine (NE) differentiation in tumors of the prostate or in the setting of prostate cancer (PCa) is rare. A survey of these lesions is presented, including usual PCa with focal NE marker-positive cells, Paneth cell-like change, prostatic 'carcinoid', high-grade NE carcinoma, as well as other tumors that do not fit neatly into these categories. The most significant clinical and pathologic features, emerging molecular evidence and the importance of differentiating NE tumors involving the prostate from secondary involvement are highlighted.

Neuroendocrine and Aggressive-Variant Prostate Cancer

“…The mixed NE carcinoma-acinar adenocarcinoma included in the PCF meeting classification, is not considered a distinct entity per the 2016 WHO classification [39]. Adenocarcinoma with Paneth cell NE differentiation, which is also included only in the PCF meeting classification, is an entity with incompletely understood clinical significance, with the limited available data pointing to an overall favorable prognosis [40].…”

Editorial Comment to Prostate carcinoma with neuroendocrine differentiation successfully treated by early detection with imaging examination

“…In this case, Kobayashi et al could diagnose potential prostate cancer with extremely low PSA value using conventional magnetic resonance imaging. 1 Apart from the usual imaging study, computed tomography with Ga-[DOTA-Tyr]-octreotate (Ga-DOTA-TATE), a somatostatin analog that binds somatostatin receptor 2 with high affinity plays a role in evaluating the presence and/or extent of NECAP. 2 Hence, NECAP that presents in the heterogeneous tissue of the prostate gland should be differentiated from the usual adenocarcinoma.…”

Loss of EHF facilitates the development of treatment-induced neuroendocrine prostate cancer

“…This phenotype reprogramming occurs through lineage plasticity, a biological process mediated, in part, by the pluripotency transcriptional factor SOX2, and facilitates cellular proliferation, metastasis, and drug resistance [10][11][12][13][14] . Histologically, treatment-related NEPC (t-NEPC) tumors present as pure small cell morphology or diversity morphologies with both small cells and adenocarcinoma cells mixed 8,9,15 . t-NEPC tumors universally express NE makers such as enolase 2 (ENO2), chromogranin A (CHGA), and synaptophysin (SYP), and exhibit an ARindependent state characterized by reduced or none AR expression 8,9,15 .…”

“…Histologically, treatment-related NEPC (t-NEPC) tumors present as pure small cell morphology or diversity morphologies with both small cells and adenocarcinoma cells mixed 8,9,15 . t-NEPC tumors universally express NE makers such as enolase 2 (ENO2), chromogranin A (CHGA), and synaptophysin (SYP), and exhibit an ARindependent state characterized by reduced or none AR expression 8,9,15 . Therefore, patients developing t-NEPC react indolently to AR-targeted therapies and have to be treated with platinum-based cytotoxic agents.…”