Table 1.

Common molecular alteration in the pathogenesis of small-cell neuroendocrine cancer of the prostate

Tumor suppressors

RB1 protein/allelic loss (85–96%)

TP53 allelic loss/mutation (60–100%)

PTEN protein/allelic loss (29–63%)

Prostate luminal epithelial markers

AR protein loss (83–100%)

PSA protein loss (81–100%)

P501s protein loss (72%)

Neuroendocrine elements and polypeptide hormones

Chromogranin A and/or synpatophysin and/or CD56 protein expression (92–100%)

Bombesin protein expression (88%)

Neural progenitor transcription factors

MYCN amplification (40–86%)

ASCL1 protein expression

Cell cycle/mitosis markers

AURKA amplification/protein expressiona (40–86%)

UBE2C protein expression (96%)

Genomic alterations

Increased number of genomic amplifications and deletions

TMPRSS2:-ERG gene rearrangements (46–86%)

AR, androgen receptor; ASCL1, achaete-scute homolog 1. ^a AURKA and MYCN amplification are concurrent in 90% of the reported cases.