Role of chromosomal loss in the progression of prostate cancers

被引：9

作者：

Ichikawa T. ^{[1
]}

Suzuki H. ^{[1
]}

Ito H. ^{[1
]}

机构：

[1] Department of Urology, Chiba University School of Medicine, 1-8-1 Inohana, Chiba 260-8670, Chuo-ku

来源：

International Journal of Clinical Oncology | 2000年 / 5卷 / 6期

关键词：

Chromosome; Loss of heterozygosity; Metastasis suppressor gene; Prostate cancer; Tumor suppressor gene;

D O I：

10.1007/PL00012062

中图分类号：

学科分类号：

摘要：

Cytogenetic, molecular cytogenetic, and molecular studies of prostate cancer have produced a large volume of data about chromosomal loci that are aberrant in prostate cancer. The cumulative data on prostate cancer reveal allelic losses on chromosome arms 2q, 3p, 5q, 6q, 7q, 8p, 9p, 10p, 10q, 11p, 11q, 12p, 13q, 16q, 17p, 17q, 18q, and 21q, but there is a great deal of variability between studies. In most cases, the frequency of allelic loss is higher in metastatic tissues or hormone-refractory tumors than in primary tumors. There also seem to be discrepancies in the genetic findings depending on methods employed. Molecular genetic studies, using polymerase chain reaction (PCR) analysis of microsatellite markers, demonstrated allelic loss at 7q31.1, whereas fluorescence in situ hybridization analysis showed a gain at the same region. Common sites of allelic loss that are consistently observed by various methods seem to exist on chromosome arms 8p, 10q, 13q, and 16q. PTEN/MMAC1 has been identified on 10q23.3 and was found to be frequently mutated in advanced prostate cancer. Other regions are also considered to harbor genes associated with the development and progression of prostate cancer, and these could be included in the diagnostic methods for the substaging of prostate cancer.

引用

页码：345 / 354

页数：9

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