希伯来大学研究团队发现，癌细胞通过超级增强子驱动生长相关基因进行极端活动，这种高强度运作导致DNA双链断裂集中出现在被超级增强子控制的基因中[1]。由博士生Osama Hidmi在教授Rami Aqeilan指导下开展的这项研究已发表于《Science Advances》期刊2026年第12卷第4期[1]。
Rami Aqeilan教授解释了这一现象的机制："癌细胞依赖超级增强子使生长基因以高速运行。我们发现这种高输出活动会对DNA造成真实压力，造成断裂热点，细胞必须反复修复。"[1]癌细胞每次修复这些DNA断裂时都可能引入错误，从而导致突变不断积累[1]。
研究表明，这种看似自我伤害的机制可能成为肿瘤进化的推动力。Osama Hidmi指出："因为癌细胞依赖这些高应力DNA区域保持生长，它们在那里可能也更脆弱。这为针对肿瘤存活所依赖的过程的治疗打开了大门。"[1]这一发现为开发新型癌症治疗方法提供了潜在靶点[1]。
Researchers at the Hebrew University have discovered that cancer cells drive their growth through a mechanism of self-inflicted DNA damage. The study, conducted by doctoral student Osama Hidmi under the supervision of Professor Rami Aqeilan and published in Science Advances volume 12, issue 4 of 2026, reveals that super-enhancers—regulatory DNA sequences that control gene expression—push growth-related genes to operate at extreme levels [1]. This intense activity causes DNA double-strand breaks to concentrate in regions controlled by these super-enhancers [1].
The findings suggest that while cancer cells rely on super-enhancers to maintain their rapid growth, this dependence comes with a hidden vulnerability. As Professor Aqeilan explained, cancer cells must run growth genes at high speed through super-enhancers, and this high-output activity "puts real stress on DNA, creating hotspots of breaks that the cell must repeatedly repair" [1]. Each repair cycle introduces the potential for errors, allowing mutations to accumulate and tumors to evolve [1]. According to Hidmi, the paradox presents a therapeutic opportunity: since cancer cells depend on these high-stress DNA regions for survival, "they may also be more fragile there, opening the door to treatments targeting the processes on which tumor survival relies" [1].