在腫瘤細胞中的DNA複製，一般會伴隨著複製叉的拖延和崩潰，以及應答DNA損傷和未成熟有絲分裂的信號通路激活，這些過程統稱為"複製應激"。發表於《自然評論:藥物發現》(Nature reviews. Drug discovery)2015年6月的一篇文章，對利用複製應激治療癌症進行了介紹，該研究成果已經取得進展，增加了研究者對於調節複製應激過程的分子機製的理解，同時，也為通過增強複製應激開發癌症治療手段提供了大量機會。除了延遲癌細胞周期發展，利用複製應激治療癌症的治療方法還可以進一步放開周期檢驗點，增加複製應激，最終誘導細胞增殖的失敗，從而達到殺傷癌細胞治療癌症的目的。

在這篇綜述文章中，作者對目前的相關研究進展進行了總結，對複製應激過程進行了係統性介紹，提出將藥物進行聯合使用或與傳統的化療方法結合可進一步促進DNA複製應激。

Exploiting replicative stress to treat cancer.

DNA replication in cancer cells is accompanied by stalling and collapse of the replication fork and signalling in response to DNA damage and/or premature mitosis; these processes are collectively known as 'replicative stress'. Progress is being made to increase our understanding of the mechanisms that govern replicative stress, thus providing ample opportunities to enhance replicative stress for therapeutic purposes. Rather than trying to halt cell cycle progression, cancer therapeutics could aim to increase replicative stress by further loosening the checkpoints that remain available to cancer cells and ultimately inducing the catastrophic failure of proliferative machineries. In this Review, we outline current and future approaches to achieve this, emphasizing the combination of conventional chemotherapy with targeted approaches.