Chromosomal Changes in Incidental Prostatic Carcinomas Detected by Comparative Genomic Hybridization

• Published in: European urology Vol. 41; no. 3; pp. 328 - 334
• Main Authors: Wolter, Hubertus, Trijic, Danilo, Gottfried, Hans-Werner, Mattfeldt, Torsten
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier B.V 01.03.2002; Elsevier
• Subjects: Aged; Biological and medical sciences; Categories T1a and T1b; Chromosome Aberrations; Comparative genomic hybridization; Humans; Incidental prostatic carcinoma; Loss of heterozygosity; Male; Medical sciences; Nephrology. Urinary tract diseases; Nucleic Acid Hybridization; Prostatic Neoplasms - diagnosis; Prostatic Neoplasms - genetics; Proto-oncogenes; Tumor suppressor genes; Tumors of the urinary system; Urinary tract. Prostate gland; Incidental prostatic carcinoma; Tumor suppressor genes; Categories T1a and T1b; Comparative genomic hybridization; Loss of heterozygosity; Proto-oncogenes; Human; Urinary system disease; Carcinoma; Prostate disease; Stage classification; Chromosome; Malignant tumor; Hybridization; Heterozygosity; Tumor progression; Genetics; Male genital diseases; Prostate; Comparative study; Tumor suppressor gene
• ISSN: 0302-2838; 1873-7560
• DOI: 10.1016/S0302-2838(02)00035-0

Objectives: The genetic changes underlying the development and progression of prostate cancer are poorly understood. To identify chromosomal regions in incidental prostatic carcinoma (T1a and T1b) was the primary aim of this study. Materials and Methods: We used comparative genomic hybridization (CGH) to search for DNA sequence copy number changes on a series of 48 T1 prostate cancer diagnosed by transurethral resection (TURP) and by adenomectomy. Incidental prostatic carcinomas have not been studied by CGH previously. Results: CGH analysis indicated that 14 cases (29.2%) of incidental prostatic carcinoma showed chromosome alterations. The most frequent alterations were chromosomal losses of 8p (10.4%), 13q (6.3%), 5q (4.2%) and 18q (4.2%), and gains of 17p (10.4%), 17q (10.4%), 9q (6.3%) and 7q (4.2%). Minimal overlapping chromosomal regions of loss, indicative for the presence of tumor suppressor genes (TSGs), were mapped to 8p22 and 13q14.1-q21.3, and minimal overlapping regions of gain, indicative for the presence of oncogenes, were found at 9q34.2-qter, 17p12 and 17q24-qter. The statistical analysis displayed a significant association between chromosomal aberration detected by CGH and high Gleason score ( P<0.005) as well as between tumor categories T1a and T1b and chromosomal imbalance ( P=0.041). Conclusions: Studies directed at incidental prostatic carcinomas allow discovery of chromosomal changes in small and highly malignant tumors. Our results suggest that loss or gain of DNA in these regions are important in prostate cancer. This is the first study, which documents the spectrum of chromosomal changes in incidental prostatic carcinomas.