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利用荧光原位杂交技术对前列腺癌8号染色体短臂进行缺失图谱分析。

Deletion mapping of chromosome 8p in prostate cancer by fluorescence in situ hybridization.

作者信息

Matsuyama H, Pan Y, Skoog L, Tribukait B, Naito K, Ekman P, Lichter P, Bergerheim U S

机构信息

Department of Urology, Karolinska Hospital, Stockholm, Sweden.

出版信息

Oncogene. 1994 Oct;9(10):3071-6.

PMID:8084616
Abstract

Double-target fluorescence in situ hybridization (FISH) was applied to 42 cases of prostate cancer and seven cases of histologically proven benign prostate hyperplasia for the detection of structural aberrations of chromosome 8. Cosmid probes for two chromosome 8p loci (LPL/8p22 and D8S7/8p23) were used in 34 specimens of malignant tumors obtained by the touch biopsy technique. Deletion was defined as when the number of cosmid signals was lower than the number of centromere signals in more than 35% of all nuclei observed. In total, thirty of the 42 (71%) specimens demonstrated any type of 8p deletion. Out of the 34 cases in which deletion mapping could be evaluated, distal deletion (D8S7) was detected in 17 (50%), of which 10 also showed deletion of LPL. Deletion of LPL was detected in 18 cases (53%), of which 8 (24%) retained the D8S7 (interstitial deletion). When the deletion pattern was graded as (1) no deletion (2) partial deletion (either D8S7 or LPL deleted) and (3) both deletions, the degree of deletion was well correlated with the tumor grade (P = 0.0009) and with stage (P = 0.0072, Fisher's Exact test). These data support the hypothesis that tumor suppressor gene(s) may be located in the chromosomal region 8p22, hence 8p deletions may play a crucial role in the pathogenesis of prostate cancer.

摘要

采用双靶点荧光原位杂交(FISH)技术对42例前列腺癌患者及7例经组织学证实的良性前列腺增生患者进行检测,以观察8号染色体的结构畸变情况。使用针对两个8号染色体短臂位点(LPL/8p22和D8S7/8p23)的黏粒探针,对通过触摸活检技术获取的34例恶性肿瘤标本进行检测。当在超过35%的观察细胞核中,黏粒信号数量低于着丝粒信号数量时,定义为缺失。42例标本中共有30例(71%)出现了任何类型的8p缺失。在34例可评估缺失图谱的病例中,17例(50%)检测到远端缺失(D8S7),其中10例同时显示LPL缺失。18例(53%)检测到LPL缺失,其中8例(24%)保留了D8S7(中间缺失)。当将缺失模式分为(1)无缺失、(2)部分缺失(D8S7或LPL缺失)和(3)两者均缺失时,缺失程度与肿瘤分级(P = 0.0009)和分期(P = 0.0072,Fisher精确检验)密切相关。这些数据支持以下假说:肿瘤抑制基因可能位于染色体区域8p22,因此8p缺失可能在前列腺癌的发病机制中起关键作用。

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