AbstractWe used the fluorescence in situ hybridization (FISH) method to show that chromosome 7 trisomy is associated with the progression of human prostate cancer. Thirty‐six specimens including 15 primary prostate carcinomas, 16 metastatic lesions, and 5 normal prostate tissues, as well as 2 prostate carcinoma cell lines of different tumorigenic potential, were examined for chromosome 7 aneuplaidy. Our results showed that the androgen‐unresponsive tumorigenic cell line PC‐3 exhibited a significantly higher ratio of chromosome 7 to total chromosome number than the androgen‐responsive nontumorigenic cell line LNCaP (P = 0.001). In prostate specimens, the frequency of trisomy 7 cells was significantly increased (P<0.05) in the advanced stage tumors (C and D1) but not in the early (6) stage tumors or normal prostatic tissue. Furthermore, metastases showed a higher frequency of trisomy 7 cells than primary tumors (P = 0.005). In 2 patients with paired primary and metastatic tumors, trisomy 7 cells increased from 4‐7% in the primary tumors to 42‐45% in the metastatic tumor cells in the bone marrow. Therefore, our data suggest that trisomy 7 may be a common feature associated with local and metastatic progression and serve as a novel marker for human prostate cancer progression. Genes Chrom Concer 9:/9‐27 (1994). © 1994 W