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CTNNB1
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Interpretation 296
Tier 3
CTNNB1
Variants
Primary Sites
Lung
Tumor Types
Non-Small Cell Lung Carcinoma
Interpretation

The cytoplasmic β-catenin protein is implicated as a cell-cell adhesion regulator coupled with cadherin and is considered as a member in the wingless/Wnt signal transduction pathway. Mutations in CTNNB1, the gene encoding β-catenin, tend to impact or even eliminate APC-dependent serine and threonine phosphorylation sites in exon 3, resulting in oncogenic stabilization of the protein. Increased protein within the nuclei serves as a transcriptional factor through binding to the Tcf/Lef family. Mutations in the β-catenin gene are uncommon in NSCLC occurring in about 1-4% of the cases. Nuclear accumulation of β-catenin was found to be associated with EGFR mutations, and β-catenin overexpression was associated with NSCLC cell line resistance to gefitinib. Wnt pathway inhibitors are in preclinical development or have entered early clinical trials. Because high β-catenin expression has been associated with good outcome rather than with poor outcome in NSCLC patients, it could potentially prove important to target specific downstream β-catenin functions rather than using agents that could directly suppress β-catenin levels through upstream targeting of the Wnt pathway.

Citations
  1. Shigemitsu K, et al. Genetic alteration of the beta-catenin gene (CTNNB1) in human lung cancer and malignant mesothelioma and identification of a new 3p21.3 homozygous deletion. Oncogene 2001;20(31):4249-57
  2. Mazieres J, et al. Wnt signaling in lung cancer. Cancer Lett 2005;222(1):1-10
  3. Stewart DJ Wnt signaling pathway in non-small cell lung cancer. J Natl Cancer Inst 2014;106(1):djt356
Last updated: 2016-08-01 19:47:33 UTC
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When using PMKB, please cite: Huang et al., JAMIA 2017


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