Prostate cancer is a heterogeneous disease whose progression is linked to genome instability. However the impact of this instability on the three-dimensional chromatin organization and how this drives progression is unclear. Using primary benign and tumour tissue, we find a high concordance in the higher-order three-dimensional genome organization across normal and prostate cancer cells. This concordance argues for constraints to the topology of prostate tumour genomes. Nonetheless, we identify changes to focal chromatin interactions and show how structural variants can induce these changes to guide cis-regulatory element hijacking. Such events result in opposing differential expression on genes found at antipodes of rearrangements. Collectively, our results argue that cis-regulatory element hijacking from structural variant-induced altered focal chromatin interactions overshadows higher-order topological changes in the development of primary prostate cancer.

中文翻译：

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结构变异的顺式调节元件劫持掩盖了原发性前列腺癌的高阶拓扑变化。

前列腺癌是一种异质性疾病，其进展与基因组不稳定性有关。然而，这种不稳定性对三维染色质组织的影响及其如何驱动进展尚不清楚。使用原发性良性和肿瘤组织，我们在正常和前列腺癌细胞的高阶三维基因组组织中发现了高度一致性。这种一致性主张对前列腺肿瘤基因组拓扑结构的限制。尽管如此，我们确定了局部染色质相互作用的变化，并显示了结构变异体如何诱导这些变化来指导顺式调控元件的劫持。此类事件导致在重排对映体上发现的基因出现相反的差异表达。总的来说，