Chromosomal anomalies in prostatic intraepithelial neoplasia and carcinoma detected by fluorescence in situ hybridization.
Chromosomal anomalies in prostatic intraepithelial neoplasia and carcinoma detected by fluorescence in situ hybridization.
复制标题
DOI：
--
复制
发表时间：
1995-11
期刊：
影响因子：
11.2
通讯作者：
J. Qian;D. Bostwick;Satoru Takahashi;T. Borell;J. Herath;M. Lieber;Robert B. Jenkins
中科院分区：
文献类型：
--
作者：
J. Qian;D. Bostwick;Satoru Takahashi;T. Borell;J. Herath;M. Lieber;Robert B. Jenkins
高级别前列腺上皮内瘤（PIN）、前列腺癌和转移瘤之间的发病关系尚不清楚。我们使用荧光原位杂交（FISH）与染色体7，8，10，12和Y的着丝粒特异性探针，以评估PIN（68个病灶），局限性前列腺癌（78个病灶），淋巴结转移（8个病灶）在40个整体安装根治性前列腺癌切除术和盆腔淋巴结切除术标本的染色体数目异常。PIN、癌和转移灶的染色体异常率分别为50%、51%和100%。PIN、癌和转移瘤的平均异常染色体数分别为0.66、1.09和3.75。PIN中最常见的异常是8号染色体的增加（32%的病灶），其次是10号（13%）、7号（10%）、12号（4%）和Y（4%）的增加。癌灶中最常见的异常是7号和8号染色体的增加（分别占癌灶的28%和30%），其次是10号（23%）、12号（9%）和Y（9%）的增加。8号染色体的增加与病理分期及Gleason评分呈正相关（P均< 0.05）。通常情况下，癌灶包含更多的异常比成对的PIN病灶，但5例前列腺包含一个或多个PIN病灶的异常比癌。在转移瘤的病例中，通常一个或多个原发肿瘤病灶与匹配的转移瘤共享染色体异常。我们的研究结果表明，PIN和前列腺癌病灶具有相似的染色体异常比例，但癌病灶通常有更多的改变。这一观察结果支持PIN通常是癌前体的假设，尽管有一些癌灶几乎没有或没有明显的染色体改变，而同时发生的PIN灶有多种改变。8号染色体的增加是最常见的数量变化，并且与癌症分期和分级的增加相关，这表明它可能在前列腺癌的发生和进展中发挥作用。通常，原发肿瘤的一个或多个病灶与相关的淋巴结转移共享染色体异常，这表明通常只有单个癌灶引起转移。
The pathogenetic relationship between high-grade prostatic intraepithelial neoplasia (PIN), prostatic carcinoma, and metastases is poorly understood. We used fluorescence in situ hybridization (FISH) with centromere-specific probes for chromosomes 7, 8, 10, 12, and Y to evaluate numeric chromosomal anomalies in PIN (68 foci), localized prostatic carcinoma (78 foci), and lymph node metastases (8 foci) in 40 whole-mount radical prostatectomy and pelvic lymphadenectomy specimens. Chromosomal anomalies were found in 50, 51, and 100% of the foci of PIN, carcinoma, and metastases, respectively. The mean numbers of abnormal chromosomes per focus were 0.66 in PIN, 1.09 in carcinoma, and 3.75 in metastases. The most frequent anomaly in PIN was a gain of chromosome 8 (32% of foci), followed by gains of chromosomes 10 (13%), 7 (10%), 12 (4%), and Y (4%). The most frequent anomalies in foci of carcinoma were gains of chromosomes 7 and 8 (28% and 30% of foci, respectively), followed by gains of chromosomes 10 (23%), 12 (9%), and Y (9%). There was a positive correlation of the gain of chromosome 8 with the pathological stage and Gleason score (both P < 0.05). Usually, carcinoma foci contained more anomalies than paired PIN foci, but five prostates contained one or more foci of PIN with more anomalies than carcinoma. Among the cases with metastases, usually one or more foci of the primary tumor shared chromosomal anomalies with the matched metastases. Our results indicate that PIN and prostatic carcinoma foci have similar proportions of chromosomal anomalies, but foci of carcinoma usually have more alterations. This observation supports the hypothesis that PIN is often a precursor of carcinoma, although there are some carcinoma foci that have few or no apparent chromosomal alterations, whereas concurrent PIN foci have multiple alterations. A gain of chromosome 8 was the most common numerical alteration and was associated with increasing cancer stage and grade, suggesting that it may play a role in the initiation and progression of prostatic carcinoma. Usually, one or more foci of the primary tumor shared chromosomal anomalies with associated lymph node metastases, suggesting that, often, just a single focus of carcinoma gives rise to metastases.