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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Curr Oncol Rep. 2017 May;19(5):32. doi: 10.1007/s11912-017-0593-6

Table 1. Clinical, histological and molecular characteristics of most common CRPC variants.

CRPC variant Survival Histology Molecular aberrations Ref

Neuroendocrine (NEPC) 1-2 years chromogranin (+/-),synaptophysin (+/-), AR low/absent low AR signaling, RB1 loss, TP53 loss, REST, high MYCN, AURKA, EZH2, PEG10, SRRM4, DLL3, epigenetic [19, 23-27, 33, 49, 50, 52, 60]
Small cell carcinoma 7 months Small blue/oat cells

“AR indifferent” castration resistant adenocarcinoma To be defined Adenocarcinoma, AR (+), AR signaling low, RB1 loss, TP53 loss, high EZH2 [33, 38, 39]

Intermediate atypical To be defined To be defined Mixed/overlapping molecular features with adenocarcinoma and NEPC [14, 57]

Aggressive variant 9-17 months Heterogeneous (Adenocarcinoma or NEPC) RB1, TP53, PTEN loss [51, 53-55]

Ductal 84 months High Gleason, endometrioid MMR gene alterations/hypermutation [60, 61, 63]