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
[1]  
Alers JC, 1997, LAB INVEST, V77, P437
[2]  
[Anonymous], 1980, Histological typing of prostate tumours / F. K. Mostofi, in collaboration with I. Sesterhenn
[3]   DELETION MAPPING OF CHROMOSOME-8, CHROMOSOME-10, AND CHROMOSOME-16 IN HUMAN PROSTATIC-CARCINOMA [J].
BERGERHEIM, USR ;
KUNIMI, K ;
COLLINS, VP ;
EKMAN, P .
GENES CHROMOSOMES & CANCER, 1991, 3 (03) :215-220
[4]   Functional identification of LZTS1 as a candidate prostate tumor suppressor gene on human chromosome 8p22 [J].
Cabeza-Arvelaiz, Y ;
Sepulveda, JL ;
Lebovitz, RM ;
Thompson, TC ;
Chinault, AC .
ONCOGENE, 2001, 20 (31) :4169-4179
[5]  
Cairns P, 1997, CANCER RES, V57, P4997
[6]   MAPPING OF REGIONS OF PHYSICAL DELETION ON CHROMOSOME 16Q IN PROSTATE-CANCER CELLS BY FLUORESCENCE IN-SITU HYBRIDIZATION (FISH) [J].
CHER, ML ;
ITO, T ;
WEIDNER, N ;
CARROLL, PR ;
JENSEN, RH .
JOURNAL OF UROLOGY, 1995, 153 (01) :249-254
[7]  
Dong JT, 1996, CANCER RES, V56, P4387
[8]   MUTATION OF THE MXI1 GENE IN PROSTATE-CANCER [J].
EAGLE, LR ;
YIN, XY ;
BROTHMAN, AR ;
WILLIAMS, BJ ;
ATKIN, NB ;
PROCHOWNIK, EV .
NATURE GENETICS, 1995, 9 (03) :249-255
[9]  
Elo JP, 1997, CANCER RES, V57, P3356
[10]   Rearrangement of the long arm of chromosome 10 in the prostate adenocarcinoma cell line LNCaP [J].
Ford, S ;
Gray, IC ;
Spurr, NK .
CANCER GENETICS AND CYTOGENETICS, 1998, 102 (01) :6-11