Alteration of the p53 locus in benign hyperplastic prostatic epithelium associated with high-grade prostatic adenocarcinoma.
Diagn Mol Pathol
; 3(4): 227-32, 1994 Dec.
Article
en En
| MEDLINE
| ID: mdl-7532528
Recent evidence suggests that the tumor suppressor protein, p53, protects somatic cells against the accumulation of genomic mutations. The genomes of cells lacking normal p53 function may become hypermutable, a condition that might result in the accumulation of multiple genetic alterations as the affected cells proliferate. Such cells may then become more susceptible to malignant transformation. We hypothesized that some high-grade prostate cancers might arise from foci of morphologically benign cells that had previously sustained p53 lesions. As an initial test of this hypothesis, we employed a microdissection technique to isolate morphologically benign cells within hyperplastic glands located near foci of high-grade adenocarcinoma. Genomic DNA from these cells was subjected to polymerase chain reaction amplification and single-stranded conformational polymorphism analysis for detecting alterations in the p53 locus. With use of this approach, gross alterations in the p53 locus were demonstrated in benign cells in 1 of 20 (5%) specimens harboring high-grade malignancy (Gleason grade 7 or higher). Thus, in some cases, hyperplastic prostatic epithelium harbors preneoplastic genetic alterations that could possibly give rise to high-grade malignancies.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Hiperplasia Prostática
/
Neoplasias de la Próstata
/
Adenocarcinoma
/
Genes p53
Tipo de estudio:
Risk_factors_studies
Límite:
Humans
/
Male
Idioma:
En
Revista:
Diagn Mol Pathol
Asunto de la revista:
BIOLOGIA MOLECULAR
/
PATOLOGIA
Año:
1994
Tipo del documento:
Article
Pais de publicación:
Estados Unidos