TY - JOUR
T1 - Chromosome 16 allelic loss analysis of a large set of microdissected prostate carcinomas
AU - Strup, Stephen E.
AU - Pozzatti, Rudy O.
AU - Florence, Charles D.
AU - Emmert-Buck, Michael R.
AU - Duray, Paul H.
AU - Liotta, Lance A.
AU - Bostwick, David G.
AU - Linehan, W. Marston
AU - Vocke, Cathy D.
PY - 1999/8
Y1 - 1999/8
N2 - Purpose: To perform loss of heterozygosity (LOH) analysis on chromosome 16 in 102 highly purified DNA samples isolated from one or more adenocarcinomas, prostatic intraepithelial neoplasia (PIN), and matched benign prostatic epithelium from 95 radical prostatectomy patients. Materials and Methods: Specimens were procured by microdissection of frozen tissue samples, thus ensuring that highly select pure populations of cells were obtained for DNA extraction and LOH analysis. Multiple microsatellite markers were used to determine allelic loss on chromosome 16q. Results: Overall loss on 16q was seen in 31% of the cancers, and occurred more frequently in high stage cancers than low stage cancers. In contrast, allelic loss in PIN failed to exceed 6% at any of the loci that were examined. Conclusions: These results suggest that inactivation of a putative tumor suppressor gene on 16q may be involved in the progression of some prostate cancers.
AB - Purpose: To perform loss of heterozygosity (LOH) analysis on chromosome 16 in 102 highly purified DNA samples isolated from one or more adenocarcinomas, prostatic intraepithelial neoplasia (PIN), and matched benign prostatic epithelium from 95 radical prostatectomy patients. Materials and Methods: Specimens were procured by microdissection of frozen tissue samples, thus ensuring that highly select pure populations of cells were obtained for DNA extraction and LOH analysis. Multiple microsatellite markers were used to determine allelic loss on chromosome 16q. Results: Overall loss on 16q was seen in 31% of the cancers, and occurred more frequently in high stage cancers than low stage cancers. In contrast, allelic loss in PIN failed to exceed 6% at any of the loci that were examined. Conclusions: These results suggest that inactivation of a putative tumor suppressor gene on 16q may be involved in the progression of some prostate cancers.
KW - Loss of heterozygosity
KW - Microsatellite polymorphism
KW - Prostate carcinoma
KW - Tissue microdissection
KW - Tumor suppressor gene
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U2 - 10.1016/S0022-5347(05)68631-4
DO - 10.1016/S0022-5347(05)68631-4
M3 - Article
C2 - 10411092
AN - SCOPUS:0032855830
SN - 0022-5347
VL - 162
SP - 590
EP - 594
JO - Journal of Urology
JF - Journal of Urology
IS - 2
ER -
