To detect the numerical changes of the chromosome 13 and 17, containing tumor suppressor genes (retinoblastoma gene and p53) in normal tissue, intraepithelial neoplasm and carcinoma of the prostate, the Fluorescence In Situ Hybridization
technique
with
paraffin embedded tissue was done. Materials observed in this study consisted of 14 cases of lacalized carcinoma(TBINOMO) and 1 cases of locally infiltrating cancer (TC1NOMO).
The chromosomal number changes were counted at normal tissue, intraepithelial neoplasm and neoplastic gland at the same radical prostatectomy specimen. From the 4 patients, studied prospectively, fresh cancer tissue and peripheral whole blood
were
collected for the primary culture of the cancer cells and lymphocytic culture. These cultured cells were used for karyotyping.
@ES The results were as follows:
@EN 1. There were no significant chromosomal number changes between 13 and 17 in each group.
2. The normal non-neoplastic duct, intraepithelial neoplasm and neoplastic gland of experimental group showed no significant difference in chromosomal change.
3. There were significant changes more than 30% in chromosomal numbers between control Y chromosome and experimental chromosome 13 and 17 in each group.
4. The karyotyping on primary cultured prostate cancer cells and lymphocyte showed significant difference in chromosomal number in spite of the same host, representing local chromosomal changes.
5. With the results collected from this study, chromosomal aberration in number in prostate biopsy would represent the already established initiation of the cancerous change in prostate and chromosomal aberration detection would be a good early
diagnostic modality to detect the high risk group who will develop the prostate cancer.
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