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Re‐expression of E‐cadherin, α‐catenin and β‐catenin, but not of γ‐catenin, in metastatic tissue from breast cancer patients
Author(s) -
Bukholm I. K.,
Nesland J. M.,
BørresenDale A.L.
Publication year - 2000
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(200001)190:1<15::aid-path489>3.0.co;2-l
Subject(s) - catenin , immunohistochemistry , cadherin , metastatic breast cancer , cyclin d1 , metastasis , pathology , cancer research , cancer , breast cancer , cell adhesion molecule , medicine , biology , cell , wnt signaling pathway , cell cycle , immunology , signal transduction , biochemistry , genetics
Abstract Tumour cell invasion and metastasis are the processes which kill most cancer patients. Tumour cells with the greatest invasive and metastatic capacity may be those with the highest number of genetic aberrations. The present study has analysed the expression of several tumour‐related proteins in both primary tumours and metastatic lesions from 34 breast cancer patients. Protein expression of p53, bcl‐2, p21, cyclin D1, E‐cadherin, α‐catenin, β‐catenin, and γ‐catenin was investigated by immunohistochemistry (IHC) using monoclonal antibodies. Metastatic tissue showed a different expression profile from the primary tumour in most patients. The most significant finding was the re‐expression of E‐cadherin, α‐catenin, and β‐catenin, and increased down‐regulation of γ‐catenin, in metastatic lesions. These results demonstrate that tumour cells, when released from the primary site and after regrowth elsewhere, are capable of re‐expression of adhesion molecules. γ‐catenin may play a different role in metastatic lesions than in primary tumours, since it is selectively down‐regulated in tumour tissue at the metastatic site. Copyright © 2000 John Wiley & Sons, Ltd.