Brookman-Amissah N, Duchesnes C, Williamson M P, Wang Q, Ahmed A, Feneley M R, Mackay A, Freeman A, Fenwick K, Iravani M, Weber B, Ashworth A, Masters J R
Prostate Cancer Research Centre, Institute of Urology, University College London, London, UK.
Prostate Cancer Prostatic Dis. 2005;8(4):335-43. doi: 10.1038/sj.pcan.4500826.
Copy number alterations in a matched pair of benign epithelial and prostate cancer cell lines derived from the same patient were assessed using array-based comparative genomic hybridisation (aCGH). The cancer cell line showed a gain of chromosome 7, deletion of chromosome 8, gains (including high level) and losses on chromosome 11, loss of 18p and gain of 20q. Deletions on chromosome 8 were confirmed with microsatellite markers. The aCGH results were compared to gene expression data obtained using DNA microarrays and suggested the involvement of caspases and ICEBERG on 11q and E2F1 on chromosome 20q.
使用基于芯片的比较基因组杂交技术(aCGH)评估了来自同一患者的一对匹配的良性上皮细胞系和前列腺癌细胞系中的拷贝数改变。癌细胞系显示7号染色体增加、8号染色体缺失、11号染色体有增加(包括高水平增加)和缺失、18p缺失以及20q增加。8号染色体上的缺失通过微卫星标记得到证实。将aCGH结果与使用DNA微阵列获得的基因表达数据进行比较,结果表明胱天蛋白酶和ICEBERG基因与11q相关,E2F1基因与20q染色体相关。