Expression of E-cadherin and its relation to the p53 protein status in human breast carcinomas

In breast carcinomas the TP53 gene is altered in 10-30% of cases. Alteration of the gene may lead to a general genomic instability, detected as deletions and/or amplifications at the gene level, and as altered expression at the mRNA and protein level. We have demonstrated a strong association betwee...

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Published in:Virchows Archiv : an international journal of pathology Vol. 431; no. 5; pp. 317 - 321
Main Authors: BUKHOLM, I. K, NESLAND, J. M, KARESEN, R, JACOBSEN, U, BØRRESEN-DALE, A.-L
Format: Journal Article
Language:English
Published: Berlin Springer 01-11-1997
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Summary:In breast carcinomas the TP53 gene is altered in 10-30% of cases. Alteration of the gene may lead to a general genomic instability, detected as deletions and/or amplifications at the gene level, and as altered expression at the mRNA and protein level. We have demonstrated a strong association between down-regulation of E-cadherin protein expression and alterations of the p53 protein, detected as TP53 gene mutation and/or protein accumulation in tumour samples from 210 patients with breast carcinomas (P < 0.001). Investigation of allelic imbalance using microsatellite markers located near the E-cadherin locus was also performed. A higher frequency of loss of heterozygosity in the microsatellite marker closest to the E-cadherin locus was observed in samples with down-regulation of E-cadherin protein expression. A higher frequency of down-regulation of the E-cadherin protein expression was found in invasive lobular carcinomas than in invasive ductal carcinomas, although this difference was of borderline significant (P = 0.084). Cases in the present series were also immunostained for cerB-2 protein overexpression. A significant association between p53 protein accumulation and cerbB-2 protein overexpression was seen (P = 0.036). The results of the present study indicate that p53 protein may play a role in regulation of E-cadherin protein expression.
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ISSN:0945-6317
1432-2307
DOI:10.1007/s004280050105