ALLELIC LOSS OF CHROMOSOME-16Q AND CHROMOSOME-10Q IN HUMAN PROSTATE-CANCER
ALLELIC LOSS OF CHROMOSOME-16Q AND CHROMOSOME-10Q IN HUMAN PROSTATE-CANCER
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DOI：
10.1073/pnas.87.22.8751
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发表时间：
1990-11-01
影响因子：
11.1
通讯作者：
ISAACS, WB
中科院分区：
文献类型：
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作者：
CARTER, BS;EWING, CM;ISAACS, WB
近年来对常见成人肿瘤分子遗传学的研究表明，多种基因改变包括癌基因的激活和抑癌基因的失活在这些肿瘤的发病机制中起重要作用。杂合性丢失是肿瘤抑制基因失活的标志，并已被用于鉴定含有这些基因的染色体区域。我们研究了男性最常见的肿瘤前列腺癌中的等位基因丢失。 28例前列腺癌标本在11个不同的染色体臂（包括3 p、7 q、9 q、10 p、10 q、11 p、13 q、16 p、16 q、17 p和18 q）上进行了杂合性丢失检查。54%（13/24）的临床局限性肿瘤和4/4的转移性肿瘤显示至少一条染色体上的杂合性丢失。染色体16 q和10 q表现出最高频率的杂合性丢失，30%的肿瘤显示这些染色体的丢失。这些数据表明，等位基因丢失是一个常见的事件，在前列腺癌，并建议，染色体16 q和10 q可能包含的网站的肿瘤抑制基因在人类前列腺癌的发病机制中的重要性。
Recent advances in understanding the molecular genetics of common adult tumors have indicated that multiple genetic alterations including the activation of oncogenes and the inactivation of tumor suppressor genes are important in the pathogenesis of these tumors. Loss of heterozygosity is a hallmark of tumor suppressor gene inactivation and has been used to identify chromosomal regions that contain these genes. We have examined allelic loss in the most common tumor in men, prostate cancer. Twenty-eight prostate cancer specimens have been examined for loss of heterozygosity at 11 different chromosomal arms including 3p, 7q, 9q, 10p, 10q, 11p, 13q, 16p, 16q, 17p, and 18q. Fifty-four percent (13/24) of clinically localized tumors and 4 of 4 metastatic tumors showed loss of heterozygosity on at least one chromosome. Chromosome 16q and 10q exhibited the highest frequency of loss of heterozygosity with 30% of tumors showing loss at these chromosomes. These data demonstrate that allelic loss is a common event in prostate cancer and suggest that chromosomes 16q and 10q may contain the sites of tumor suppressor genes important in the pathogenesis of human prostate cancer.