Gain and loss of chromosomes 1, 7, 8, 10, 18, and Y in 46 prostate cancers

被引:33
作者
Konig, JJ
Teubel, W
Romijn, JC
Schroder, FH
Hagemeijer, A
机构
[1] ERASMUS UNIV, DEPT CELL BIOL, NL-3000 DR ROTTERDAM, NETHERLANDS
[2] ERASMUS UNIV, DEPT GENET, NL-3000 DR ROTTERDAM, NETHERLANDS
关键词
fluorescence in situ hybridization; prostatic carcinoma; benign prostatic hyperplasia; DNA flow cytometry; clinical correlation;
D O I
10.1016/S0046-8177(96)90404-9
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Fluorescence in situ hybridization (FISH) with centromere probes was used to investigate numerical aberrations of chromosomes 1, 7, 8, 10, 18, and Y in 46 prostate carcinoma (PC) and 11 benign prostatic hyperplasia (BPH) samples. None of the benign specimens showed any chromosomal aberration. Forty-one of 46 PC specimens showed numerical aberrations of one or more chromosomes. All investigated chromosomes showed numerical aberrations in at least 30% of the specimens, gain being more frequent than loss. Comparison of DNA flow cytometry (FCM) and FISH results showed that not only aneuploid tumors but also most diploid tumors harbored numerical chromosome aberrations. Chromosome 10 was the most frequently gained (65%), and Y the most frequently lost chromosome (14%). Nometastatic and metastatic tumors differed significantly (P < .05) in the number of copies for chromosomes 7, 8, and 10, but not for 1, 18, and Y. These results suggest strongly that gains of chromosomes 7, 8, and 10 are involved in PC progression. Copyright (C) 1996 by W.B. Saunders Company.
引用
收藏
页码:720 / 727
页数:8
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