Prostate cancer and the genomic revolution: Advances using microarray analyses

被引:10
作者
Calvo, A
Gonzalez-Moreno, O
Yoon, CY
Huh, JI
Desai, K
Nguyen, QT
Green, JE
机构
[1] NCI, Lab Cell Regulat & Carcinogenesis, NIH, Bethesda, MD 20892 USA
[2] Univ Navarra, Ctr Appl Med Res, Div Oncol, E-31080 Pamplona, Spain
[3] Univ Navarra, Dept Histol & Pathol, E-31080 Pamplona, Spain
[4] Korea Univ, Coll Med, Dept Urol, Seoul 136701, South Korea
基金
美国国家卫生研究院;
关键词
cDNA microarrays; prostate cancer; gene expression profiling;
D O I
10.1016/j.mrfmmm.2004.08.019
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The emerging technology of microarray analysis allows the establishment of molecular portraits of prostate cancer and the discovery of novel genes involved in the carcinogenesis process. Many novel genes have already been identified using this technique, and functional analyses of these genes are currently being tested. The combination of microarray analysis with other recently developed high-throughput techniques, such as protcomics, tissue arrays, and gene promoter-methylation, especially using tissue microdissection methods, will provide us with more comprehensive insights into how prostate cancer develops and responds to gene-targeted therapies. Animal models of prostate cancer are being characterized by high throughput techniques to better define the similarities and differences between those models and the human disease, and to determine whether particular models may be useful for specific targeted therapies in pre-clinical studies. Although profiling of mRNA expression provides important information of gene expression, the development of proteomic technologies will allow for an even more precise global insight into cellular signaling and structural alterations during prostate carcinogenesis. Not only will the "omic" revolution change basic science, but it will lead to a new era of molecular medicine. Published by Elsevier B.V.
引用
收藏
页码:66 / 79
页数:14
相关论文
共 85 条
[1]   Molecular genetics of prostate cancer [J].
Abate-Shen, C ;
Shen, MM .
GENES & DEVELOPMENT, 2000, 14 (19) :2410-2434
[2]  
Amler LC, 2000, CANCER RES, V60, P6134
[3]  
Asamoto M, 2001, CANCER RES, V61, P4693
[4]  
Banks RE, 1999, ELECTROPHORESIS, V20, P689, DOI 10.1002/(SICI)1522-2683(19990101)20:4/5<689::AID-ELPS689>3.0.CO
[5]  
2-J
[6]   SUPPRESSION OF TUMORIGENICITY OF HUMAN PROSTATE CARCINOMA-CELLS BY REPLACING A MUTATED RB GENE [J].
BOOKSTEIN, R ;
SHEW, JY ;
CHEN, PL ;
SCULLY, P ;
LEE, WH .
SCIENCE, 1990, 247 (4943) :712-715
[7]   Prostatic intraepithelial neoplasia [J].
Bostwick D.G. .
Current Urology Reports, 2000, 1 (1) :65-70
[8]   Contribution of the androgen receptor to prostate cancer predisposition and progression [J].
Buchanan, G ;
Irvine, RA ;
Coetzee, GA ;
Tilley, WD .
CANCER AND METASTASIS REVIEWS, 2001, 20 (3-4) :207-223
[9]  
Calvo A, 2002, CANCER RES, V62, P5325
[10]   Methylation target array for rapid analysis of CpG island hype rmethyl ation in multiple tissue genomes [J].
Chen, CM ;
Chen, HL ;
Hsiau, THC ;
Hsiau, AHA ;
Shi, HD ;
Brock, GJR ;
Wei, SH ;
Caldwell, CW ;
Yan, PS ;
Huang, THM .
AMERICAN JOURNAL OF PATHOLOGY, 2003, 163 (01) :37-45