Clinical significance of chromosome 8p, 10q and 16q deletions in prostate cancer

被引:43
作者
Matsuyama, H
Pan, Y
Yoshihiro, S
Kudren, D
Naito, K
Bergerheim, USR
Ekman, P
机构
[1] Yamaguchi Univ, Sch Med, Dept Urol, Ube, Yamaguchi 7558505, Japan
[2] Karolinska Hosp, Dept Urol, S-10401 Stockholm, Sweden
关键词
fluorescence in situ hybridization (FISH); disease progression; tumor suppressor gene;
D O I
10.1002/pros.10173
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND. We lack simple and reliable diagnostic tools to predict pathological staging as well as further progression of prostate cancer in individual cases. METHODS. We studied deletions on 8p (8p22 and 8p23-pter), 10q (10q24-qter), and 16q (16q24) by fluorescence in situ hybridization in 53 specimens from patients with prostate cancer, and compared the status of these deletions with various clinical parameters. Forty-five cases were further evaluated regarding disease progression with a median follow-up period of 62 months. RESULTS. The overall frequencies of deletions for 8p, 10q, and 16q were 74, 55, and 55%, respectively. The frequency of 8p and 16q deletions increased significantly in parallel with tumor grade (P < 0.01 and < 0.05, respectively), while that of 10q deletions did not. Patients whose tumors showed 8p22 deletions had a significantly higher frequency in pT3 or metastatic tumors than in pT2 tumors. Patients whose tumors showed both 8p22 and 16q24 deletions had a significantly higher frequency of nodal metastases than non-metastases. A Cox hazard proportional model revealed 8p22 deletion to be the strongest parameter predictive of disease progression (hazard ratio = 6.624; P = 0.0001). CONCLUSION. Estimation of 8p22 and 16q24 deletions may serve as a genetic diagnosis for predicting pathological staging as well as disease progression in prostate cancer. (C) 2002 Wiley- Liss, Inc.
引用
收藏
页码:103 / 111
页数:9
相关论文
共 38 条
[31]   Prostate-specific antigen after radiation therapy - Prognosis by pretreatment level and post-treatment nadir [J].
Schellhammer, PF ;
ElMahdi, AM ;
Kuban, DA ;
Wright, GL .
UROLOGIC CLINICS OF NORTH AMERICA, 1997, 24 (02) :407-+
[32]   ANX7, a candidate tumor suppressor gene for prostate cancer [J].
Srivastava, M ;
Bubendorf, L ;
Srikantan, V ;
Fossom, L ;
Nolan, L ;
Glasman, M ;
Leighton, X ;
Fehrle, W ;
Pittaluga, S ;
Raffeld, M ;
Koivisto, P ;
Willi, N ;
Gasser, TC ;
Kononen, J ;
Sauter, G ;
Kallioniemi, OP ;
Srivastava, S ;
Pollard, HB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (08) :4575-4580
[33]  
Suzuki H, 1996, GENE CHROMOSOME CANC, V17, P225, DOI 10.1002/(SICI)1098-2264(199612)17:4<225::AID-GCC4>3.3.CO
[34]  
2-S
[35]  
Suzuki H, 1998, CANCER RES, V58, P204
[36]  
TAKAHASHI S, 1994, CANCER RES, V54, P3574
[37]   THE INCIDENCE AND SIGNIFICANCE OF DETECTABLE LEVELS OF SERUM PROSTATE-SPECIFIC ANTIGEN AFTER RADICAL PROSTATECTOMY [J].
TRAPASSO, JG ;
DEKERNION, JB ;
SMITH, RB ;
DOREY, F .
JOURNAL OF UROLOGY, 1994, 152 (05) :1821-1825
[38]  
Washburn JG, 2000, CLIN CANCER RES, V6, P4647