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DNA fingerprint detection of somatic mutations in benign prostatic hyperplasia and prostatic adenocarcinoma

Genetic alterations within diseased prostate tissue were analysed by genomic DNA fingerprinting using a minisatellite probe (lambda 33.6), a simple repetitive oligonucleotide probe (GTG)5, and an additional human multilocus probe (pV47‐2). In prostatic adenocarcinoma, somatic mutations were detected in 77% of the samples compared with 38% of the benign prostatic hyperplasia samples. No correlation was evident with either the tissue histopathology or the grading or staging classification of the malignant tissue. Because one of the probes (pV47‐2) did not demonstrate any changes in the tumour tissue, and because the probes exhibited specificity for different regions of the genome, it is possible to conclude that mutations occur widely throughout the genome, perhaps with the exception of certain domains. The results suggest that somatic mutations accompany the development of both benign and malignant pathologies of the prostate. Furthermore, benign prostatic hyperplasia should be considered as a risk indicator for processes leading to prostatic adenocarcinoma. Genes Chromosom Cancer 17:31–36 (1996). © 1996 Wiley‐Liss, Inc.