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ErbB2 signaling

Candidate: concept label1 source documents5 linked claims
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Evidence Snippets

Increased ErbB2 signaling is a rapid adaptation to ASI and contributes to castration resistance.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1expression changesupports2025Source 1DOIPubMed

d16ERBB2 is increased after androgen signaling inhibition and contributes to increased ErbB2 signaling.

Quoted textsource-backed
Overexpression of an active ERBB2 splice variant (d16ERBB2) was also increased rapidly after ASI in prostate cancer cells and was found in a subset of CRPC. Increases in NRG1 and d16ERBB2 contribute to increased ErbB2 signaling.
Claim 2expression changesupports2025Source 1DOIPubMed

NRG1 is increased after androgen signaling inhibition and contributes to increased ErbB2 signaling.

Quoted textsource-backed
The ErbB3/ErbB2-activating ligand NRG1 was found by IHC in ∼75% of neoadjuvant-treated tumors. NRG1 mRNA was rapidly increased by ASI in prostate cancer cells and xenografts and was increased in post-ASI data sets. Increases in NRG1 and d16ERBB2 contribute to increased ErbB2 signaling.
Claim 3mechanistic rolesupports2025Source 1DOIPubMed

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.
Claim 4prevalencesupports2025Source 1DOIPubMed

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.
Claim 5therapeutic responsesupports2025Source 1DOIPubMed

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.