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Interpretation 265
Tier 3
CTNNB1
Variants
Primary Sites
Prostate
Tumor Types
Adenocarcinoma
Interpretation

Beta catenin is a transcriptional co-regulator and an adapter protein for cellular adhesion; it comprises part of the Wnt signaling pathway and intracellular levels of beta-catenin are regulated by its phosphorylation, ubiquitination and proteosomal degradation. Accumulation of nuclear beta catenin can lead to a tumoral phenotype and oncogenic transformation in a variety of solid tumors. Various oncogenic mutants of beta catenin have been found in different tumor types which alter its degradation, leading to its accumulation and promoting tumor growth. CTNNB1 mutations in prostate cancer occur rarely, in only 2-5% of cases. Currently, the function of β-Catenin in human prostate cancer continues to be explored. In the context of prostate, β-Catenin may modulate the androgen receptor (AR) pathway. Some preclinical mouse studies have shown that increased β-Catenin levels can cooperate with PTEN loss to promote the progression of aggressive invasive prostate cancer together with squamous metaplasia. Clinical correlation is recommended.

Citations
  1. Cancer Genome Atlas Research Network The Molecular Taxonomy of Primary Prostate Cancer. Cell 2015;163(4):1011-25
  2. Gerstein AV, et al. APC/CTNNB1 (beta-catenin) pathway alterations in human prostate cancers. Genes Chromosomes Cancer 2002;34(1):9-16
  3. Sidaway P Prostate cancer: Wnt signalling induces resistance. Nat Rev Urol 2015;12(11):597
  4. Yardy GW, et al. Wnt signalling and prostate cancer. Prostate Cancer Prostatic Dis 2005;8(2):119-26
  5. Francis JC, et al. b-catenin is required for prostate development and cooperates with Pten loss to drive invasive carcinoma. PLoS Genet 2013;9(1):e1003180
Last updated: 2016-05-05 13:29:28 UTC
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When using PMKB, please cite: Huang et al., JAMIA 2017


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