Abstract
We studied the relevance of adenomatous polyposis coli (APC)/beta-catenin signalling in the development of breast cancer by analysing the expression of beta-catenin in 54 primary breast tumours (34 ductal and 20 lobular). We showed that 13% of the tumours exhibited upregulated levels of beta-catenin in the cytosol suggesting that defects in APC/beta-catenin signalling components had lowered the rate of beta-catenin degradation. No mutations were observed in the amino-terminal region of beta-catenin, which comprises conserved serine residues important for phosphorylation-dependent degradation of the protein, but the APC protein was altered in 6% of the tumours. Tyrosine phosphorylation of beta-catenin was detected in only one tumour and could, therefore, not have been responsible for the observed increased levels of this protein. Although 9% of the tumours displayed upregulation of c-MYC protein, there was no correlation with beta-catenin overexpression, suggesting that increased beta-catenin expression is not the major cause of c-myc gene activation in breast cancer. It is imperative that elements that selectively drive the oncogenic activity of beta-catenin in breast cancer be identified.
Original language | English |
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Pages (from-to) | 242-8 |
Number of pages | 7 |
Journal | European Journal of Cancer |
Volume | 36 |
Issue number | 2 |
Publication status | Published - 2000 Jan |
Subject classification (UKÄ)
- Cancer and Oncology
Free keywords
- Adenomatous Polyposis Coli Protein
- Adult
- Blotting, Western
- Breast Neoplasms/genetics
- Carcinoma, Ductal, Breast/genetics
- Carcinoma, Lobular/genetics
- Cell Communication
- Cytoskeletal Proteins/metabolism
- Female
- Humans
- Mutation/genetics
- Neoplasm Proteins/metabolism
- Sweden
- Trans-Activators
- beta Catenin