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Involvement of adenomatous polyposis coli (APC)/beta-catenin signalling in human breast cancer

Jönsson, M LU ; Borg, A LU ; Nilbert, M LU and Andersson, T LU (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.

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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
  • scopus:0033976526
  • pmid:10741284
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
2021-09-15 04:18:48
@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},
  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},
}