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Formation of Human Prostate Epithelium Using Tissue Recombination of Rodent Urogenital Sinus Mesenchyme and Human Stem Cells
Published on: June 22, 2013
RER(+) phenotype in prostate intra-epithelial neoplasia associated with human prostate-carcinoma development
1Laboratoire de Biochimie, Unité de Biochimie Génétique, Centre Hospitalier Lyon-Sud, Pierre-Bénite, France.
International Journal of Cancer
|July 27, 1999
Summary
The mutator phenotype, a mechanism for gene inactivation, was found in 42% of prostate tumors. This early event in prostate cancer development was detected in pre-cancerous lesions, suggesting its role in tumorigenesis.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- The mutator phenotype (RER(+)) is a known mechanism for tumor suppressor gene inactivation in colorectal cancer.
- Understanding its role in prostate cancer is crucial for early detection and treatment.
Purpose of the Study:
- To determine the frequency, intratumor distribution, and timing of the mutator phenotype in prostate carcinoma.
- To investigate the association between the mutator phenotype and pre-cancerous lesions like prostate intra-epithelial neoplasia (PIN).
Main Methods:
- Analysis of ten microsatellite loci in 172 carcinoma foci (CF) and 57 associated non-cancerous prostate tissues from 60 patients.
- Comparison of RER(+) phenotype frequency in CF, PIN, and non-dysplastic hyperplastic (HP) tissues.
Main Results:
- The RER(+) phenotype was detected in 42% of prostate tumors.
- Clonal RER(+) foci were found in pre-cancerous PIN (16%) and carcinoma foci (22%), but rarely in non-dysplastic HP (4%).
- Microsatellite instability (MI) was significantly more frequent in CF and PIN compared to HP.
Conclusions:
- The mutator phenotype may occur as an early event in prostate tumorigenesis.
- RER(+) foci are significantly more frequent in carcinoma and pre-cancerous lesions than in normal prostate tissue.
- The presence of shared mutations in PIN and associated cancer suggests a progression model involving the mutator phenotype.
