Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Prostate Cancer Prostatic Dis. 2010 Jun;13(2):117-25. doi: 10.1038/pcan.2010.2. Epub 2010 Feb 23.
Our previous work identified a chromosomal translocation t(4;6) in prostate cancer cell lines and primary tumors. Using probes located on 4q22 and 6q15, the breakpoints identified in LNCaP cells, we performed fluorescence in situ hybridization analysis to detect this translocation in a large series of clinical localized prostate cancer samples treated conservatively. We found that t(4;6)(q22;q15) occurred in 78 of 667 cases (11.7%). The t(4;6)(q22;q15) was not independently associated with patient outcome. However, it occurs more frequently in high clinical T stage, high tumor volume specimens and in those with high baseline PSA (P=0.001, 0.001 and 0.01, respectively). The t(4;6)(q22;q15) occurred more frequently in samples with two or more TMPRSS2:ERG fusion genes caused by internal deletion than in samples without these genomic alterations, but this correlation is not statistically significant (P=0.0628). The potential role of this translocation in the development of human prostate cancer is discussed.
我们之前的工作在前列腺癌细胞系和原发肿瘤中鉴定出了一条染色体易位 t(4;6)。使用位于 4q22 和 6q15 的探针，我们在经过保守治疗的大量临床局限性前列腺癌样本中进行了荧光原位杂交分析，以检测该易位。我们发现，在 667 例病例中有 78 例（11.7%）存在 t(4;6)(q22;q15)。t(4;6)(q22;q15)与患者预后无关。然而，它在高临床 T 期、高肿瘤体积标本和高基线 PSA 水平的患者中更常见（P=0.001、0.001 和 0.01，分别）。在由于内部缺失而导致两个或更多 TMPRSS2:ERG 融合基因的样本中，t(4;6)(q22;q15)发生的频率高于没有这些基因组改变的样本，但这种相关性没有统计学意义（P=0.0628）。讨论了这种易位在人类前列腺癌发展中的潜在作用。
