This study sought to identify mechanisms driving increased ErbB2 activity and their role in progression to castration-resistant prostate cancer (CRPC).
First-pass extracted concept
castration-resistant prostate cancer
Candidate: concept label1 source documents4 linked claims
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Aliases
CRPC
Evidence Snippets
Supporting Sources
Linked Claims
ErbB2 phosphorylation may serve as a biomarker for tumors that will respond in CRPC.
Quoted textsource-backed
ErbB2 phosphorylation may be a biomarker for tumors that will respond in CRPC.
Increased ErbB2 signaling is a rapid adaptation to androgen signaling inhibition and contributes to castration resistance in prostate cancer.
Quoted textsource-backed
Increased ErbB2 signaling is a rapid adaptation to ASI and contributes to castration resistance.
Phospho-ErbB2-positive ErbB2 activation was present in approximately 26% of residual tumors after neoadjuvant androgen signaling inhibition and in advanced CRPC.
Quoted textsource-backed
ErbB2 activation, identified by IHC with an antibody against phosphorylated ErbB2, was present in ∼26% of residual tumors in radical prostatectomies after neoadjuvant androgen signaling inhibition (ASI) and in advanced CRPC.
Neratinib suppresses ErbB2-driven prostate cancer phenotypes, enhancing responses to castration and suppressing growth of castration-resistant xenografts with ErbB2 activation.
Quoted textsource-backed
ErbB2 signaling in all models remained sensitive to the covalent ErbB2 inhibitor neratinib, which enhanced responses to castration and suppressed the growth of castration-resistant xenografts with ErbB2 activation.