Rare histologic transformation of a CTNNB1 (β-catenin) mutated prostate cancer with aggressive clinical course.

ABSTRACT:

Background

Catenin (Cadherin-Associated Protein), Beta 1 (CTNNB1) genomic alterations are rare in prostate cancer (PCa). Gain-of-function mutations lead to overexpression of β-catenin, with consequent hyperactivation of the Wnt/β-catenin signaling pathway, implicated in PCa progression and treatment resistance. To date, successful targeted treatment options for Wnt/β-catenin - driven PCa are lacking.

Methods

We report a rare histologic transformation of a CTNNB1 (β-catenin) mutated metastatic castration resistant prostate cancer (mCRPC), clinically characterized by highly aggressive disease course. We histologically and molecularly characterized the liver metastatic tumor samples, as well as successfully generated patient-derived organoids (PDOs) and patient-derived xenograf

SUBMITTER: Akhoundova D 

PROVIDER: S-EPMC11191256 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature