APC/CTNNB1 (β-catenin) pathway alterations in human prostate cancers

Amy V. Gerstein, Teresa Acosta Almeida, Guojing Zhao, Eric Chess, Ie Ming Shih, Kent Buhler, Kenneth Pienta, Mark A. Rubin, Robert Vessella, Nickolas Papadopoulos

Research output: Contribution to journalArticlepeer-review

125 Scopus citations


Genetic alterations serve as beacons for the involvement of specific pathways in tumorigenesis. It was previously shown that 5% of prostate tumors harbor CTNNB1 mutations, suggesting that this tumor type may involve a deregulated APC/CTNNB1 pathway. To explore this possibility further, we searched for mutations in genes implicated in this pathway in 22 samples that included cell lines, xenografts, and primary tumors. We identified seven alterations: two in CTNNB1, three in APC, and two in hTRCP1 (also known as BTRC) which controls the degradation of CTNNB1. Alterations in the CTNNB1 regulatory domain, APC, and hTRCP1 were mutually exclusive, consistent with their equivalent effects on CTNNB1 stability. These results suggest that CTNNB1 signaling plays a critical role in the development of a significant fraction of prostate cancers. Moreover, they provide the first evidence that hTRCP1 plays a role in human neoplasia.

Original languageEnglish (US)
Pages (from-to)9-16
Number of pages8
JournalGenes Chromosomes and Cancer
Issue number1
StatePublished - Apr 9 2002

ASJC Scopus subject areas

  • Genetics
  • Cancer Research


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