High-resolution genome-wide copy-number analysis suggests a monoclonal origin of multifocal prostate cancer

被引:48
作者
Boyd, Lara K. [1 ]
Mao, Xueying [1 ]
Xue, Liyan [1 ,2 ,3 ]
Lin, Dongmei [1 ,2 ,3 ]
Chaplin, Tracy [4 ]
Kudahetti, Sakunthala C. [1 ]
Stankiewicz, Elzbieta [1 ]
Yu, Yongwei [5 ]
Beltran, Luis [6 ]
Shaw, Greg [7 ]
Hines, John [7 ]
Oliver, R. Tim D. [4 ]
Berney, Daniel M. [1 ]
Young, Bryan D. [4 ]
Lu, Yong-Jie [1 ]
机构
[1] Queen Mary Univ London, Ctr Mol Oncol, Barts Canc Inst, London EC1M 6BQ, England
[2] Chinese Acad Med Sci, Dept Pathol, Canc Inst Hosp, Beijing 100730, Peoples R China
[3] Peking Union Med Coll, Beijing 100021, Peoples R China
[4] Queen Mary Univ London, Ctr Haematooncol, Barts Canc Inst, London EC1M 6BQ, England
[5] Second Military Med Univ, Dept Pathol, Changhai Hosp, Shanghai, Peoples R China
[6] Whipps Cross Hosp & Chest Clin, Dept Histopathol, London, England
[7] Whipps Cross Hosp & Chest Clin, Dept Urol, London, England
基金
英国医学研究理事会;
关键词
IN-SITU HYBRIDIZATION; PAPILLARY THYROID-CARCINOMA; INTRAEPITHELIAL NEOPLASIA; CHROMOSOMAL-ANOMALIES; INDEPENDENT ORIGIN; HISTOLOGICAL GRADE; MOLECULAR ANALYSIS; CLONAL EVOLUTION; BREAST-CANCER; ALLELIC LOSS;
D O I
10.1002/gcc.21944
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Many human cancers present as multifocal lesions. Understanding the clonal origin of multifocal cancers is of both etiological and clinical importance. The molecular basis of multifocal prostate cancer has previously been explored using a limited number of isolated markers and, although independent origin is widely believed, the clonal origin of multifocal prostate cancer is still debatable. We attempted to address clonal origin using a genome-wide copy-number analysis of individual cancer and high-grade prostatic intraepithelial neoplasia (HGPIN) lesions. Using Affymetrix array 6.0 copy-number analysis, we compared the genomic changes detected in 48 individual cancer and HGPIN lesions, isolated from 18 clinically localized prostate cancer cases. Identical genomic copy-number changes, shared by all same-case cancer foci, were detected in all 13 informative cases displaying multiple tumor foci. In addition, individual HGPIN lesions in the two multifocal-HGPIN cases available shared identical genomic changes. Commonly known genomic alterations, including losses at 6q15, 8p21.3-8p21.2, 10q23.2-10q23.31, 16q22.3, 16q23.2-16q23.3 and 21q22.2-21q22.3 regions and gain of 8q24.3 were the most frequently detected changes in this study and each was detected in all same-case foci in at least one case. Microarray data were confirmed by fluorescence in situ hybridization in selected foci. Our high-resolution genome-wide copy-number data suggest that many multifocal cases derive from a single prostate cancer precursor clone and that this precursor may give rise to separate HGPIN foci and may further progress to multifocal invasive prostate cancer. These findings, which demonstrate the monoclonal origin of multifocal prostate cancer, should significantly enhance our understanding of prostate carcinogenesis. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:579 / 589
页数:11
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