RER(+) phenotype in prostate intra-epithelial neoplasia associated with human prostate-carcinoma development.
Int J Cancer
; 82(5): 635-9, 1999 Aug 27.
Article
em En
| MEDLINE
| ID: mdl-10417758
ABSTRACT
The mutator (RER(+)) phenotype has been shown to be a mutational mechanism for tumour-suppressor-gene inactivation in colorectal cancer. A group of 60 prostate-carcinoma patients was studied to determine the frequency, intratumour distribution and timing of mutator phenotype in this cancer. Ten microsatellite loci were analyzed in 172 carcinoma foci (CF) and in 57 associated non-cancerous prostate tissues, including 31 areas of prostate intra-epithelial neoplasia (PIN) and 26 non-dysplastic areas with glandular hyperplasia (HP). We detected lesions with the RER(+) phenotype in 42% (25/60) of the prostate tumours. Clonal foci with RER(+) phenotype were detected at similar frequencies in pre-cancereous PIN (16%, 5/31) as in associated carcinoma foci (22%, 37/172), but were detected in only one of the 26 non-dysplastic prostate tissues studied (4%). Thus, clonal RER(+) foci were significantly more frequent in CF than in HP (p < 0.05). MI itself was significantly more frequent in CF (53%, p < 0.0001) and in PIN (35%, p < 0.05) than in HP (12%). Furthermore, 5 PIN harboured microsatellite mutations also detected in the associated cancer. Our overall results therefore strongly suggest that the mutator phenotype may occur as an early event in prostate tumorigenesis.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Próstata
/
Neoplasia Prostática Intraepitelial
Tipo de estudo:
Risk_factors_studies
Limite:
Humans
/
Male
Idioma:
En
Revista:
Int J Cancer
Ano de publicação:
1999
Tipo de documento:
Article
País de afiliação:
França