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  • Title: Cytogenetic studies of prostatic cancer.
    Author: Lundgren R.
    Journal: Scand J Urol Nephrol Suppl; 1991; 136():1-35. PubMed ID: 1871551.
    Abstract:
    In this study we wanted to find out if the size or position of the constitutive C-band positive heterochromatin regions of chromosomes was associated with variation in prostatic cancer predisposition. We found no such association when comparing the whole patient group with healthy controls, but younger (less than 70 years) cancer patients had significantly higher frequencies of large C-bands on chromosomes 1 and 16 than older patients (greater than 70 years). This could indicate a possible relationship between the amount of constitutive heterochromatin on chromosomes 1 and 16 and susceptibility to early development of prostatic cancer. The purpose of this study was to examine if the number of AgNORs was higher in malignant than normal or hyperplastic prostatic tissue, and if the number of AgNORs increased with increasing grade of malignancy. More AgNOR dots were found in the prostatic adenocarcinomas (average 24/cell) than in the normal and hyperplastic prostates (average 13/cell). The poorly differentiated adenocarcinomas had more AgNORs than the moderately and well differentiated cancers. The data indicate that analysis of silver staining-positive material in intact interphase cells may help distinguish between benign and malignant prostatic tumors, and between highly malignant and low malignant carcinomas. The purpose was to find consistent and specific chromosome abnormalities in primary prostatic adenocarcinomas. Because then existing techniques for culturing human neoplastic prostatic tissue rarely yielded sufficiant epithelial cell growth and mitosis we decided to modify these techniques. Tumor samples from 82 patients were processed for short-term culture. Cytogenetic analysis was successful in 57 tumors, 42 of which were cultured after September 1, 1988, when the modifications were implemented. Thirteen of the 15 primary tumor samples that contained clonal karyotypic abnormalities were processed after September 1, 1988. Loss of chromosomal material from 7q, 8p, and 10q, and structural aberrations of bands 7q22 and 10q24 were the most common aberrations found. From these data it may be inferred that both loss of tumor suppressor genes and activation of oncogenes located in the breakpoint regions may be important pathogenetic events in the development or progression of prostatic adenocarcinoma. In this study we wanted to examine the clinical implications of karyotypic abnormalities. We found a significant difference in survival after diagnosis and surgery between patients whose tumors had clonal structural abnormalities (A), patients whose tumors had nonclonal changes (NA), and patients whose tumors had normal karyotypes only (N).(ABSTRACT TRUNCATED AT 400 WORDS)
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