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Key proteins involved in DDR are frequently mutated\/inactivated in human cancers and promote genomic instability, a recognized hallmark of cancer. Besides being an intrinsic property of tumors, DDR also represents a unique therapeutic opportunity. Indeed, inhibition of DDR is expected to delay repair, causing persistent unrepaired breaks, to interfere with cell cycle progression, and to sensitize cancer cells to several DNA\u2010damaging agents, such as radiotherapy and chemotherapy. In addition, DDR defects in cancer cells have been shown to render these cells more dependent on the remaining pathways, which could be targeted very specifically (synthetic lethal approach). Research over the past two decades has led to the synthesis and testing of hundreds of small inhibitors against key DDR proteins, some of which have shown antitumor activity in human cancers. In parallel, the search for synthetic lethality interaction is broadening the use of DDR inhibitors. In this review, we discuss the state\u2010of\u2010art of ataxia\u2010telangiectasia mutated, ataxia\u2010telangiectasia\u2010and\u2010Rad3\u2010related protein, checkpoint kinase 1, Wee1 and Pol\u03b8 inhibitors, highlighting the results obtained in the ongoing clinical trials both in monotherapy and in combination with chemotherapy and radiotherapy.<\/jats:p>","DOI":"10.1002\/mco2.788","type":"journal-article","created":{"date-parts":[[2024,11,1]],"date-time":"2024-11-01T05:20:09Z","timestamp":1730438409000},"source":"Crossref","is-referenced-by-count":21,"title":["Targeting the DNA damage response in cancer"],"prefix":"10.1002","volume":"5","author":[{"given":"Federica","family":"Guffanti","sequence":"first","affiliation":[{"name":"Laboratory of Preclinical Gynecological Oncology Department of Experimental Oncology Istituto di Ricerche Farmacologiche Mario Negri IRCCS  Milan 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