Involvement of adenomatous polyposis coli (APC)/beta-catenin signalling in human breast cancer
(2000) In European Journal of Cancer 36(2). p.8-242- 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... (More)
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.
(Less)
- author
- Jönsson, M LU ; Borg, A LU ; Nilbert, M LU and Andersson, T LU
- organization
- publishing date
- 2000-01
- type
- Contribution to journal
- publication status
- published
- subject
- 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
- in
- European Journal of Cancer
- volume
- 36
- issue
- 2
- pages
- 7 pages
- publisher
- Elsevier
- external identifiers
-
- pmid:10741284
- scopus:0033976526
- ISSN
- 0959-8049
- language
- English
- LU publication?
- yes
- id
- 556c7d5a-d989-427d-9bf6-ce1468df9dcb
- date added to LUP
- 2019-06-20 11:38:40
- date last changed
- 2024-05-15 13:48:38
@article{556c7d5a-d989-427d-9bf6-ce1468df9dcb,
abstract = {{<p>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.</p>}},
author = {{Jönsson, M and Borg, A and Nilbert, M and Andersson, T}},
issn = {{0959-8049}},
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}},
language = {{eng}},
number = {{2}},
pages = {{8--242}},
publisher = {{Elsevier}},
series = {{European Journal of Cancer}},
title = {{Involvement of adenomatous polyposis coli (APC)/beta-catenin signalling in human breast cancer}},
volume = {{36}},
year = {{2000}},
}