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- W2897926526 endingPage "e478s" @default.
- W2897926526 startingPage "e478s" @default.
- W2897926526 abstract "The main goal of chemotherapeutic drugs is to induce massive cell death in tumors. Cisplatin is an antitumor drug widely used to treat several types of cancer. Despite its remarkable efficiency, most tumors show intrinsic or acquired drug resistance. The primary biological target of cisplatin is genomic DNA, and it causes a plethora of DNA lesions that block transcription and replication. These cisplatin-induced DNA lesions strongly induce cell death if they are not properly repaired or processed. To counteract cisplatin-induced DNA damage, cells use an intricate network of mechanisms, including DNA damage repair and translesion synthesis. In this review, we describe how cisplatin-induced DNA lesions are repaired or tolerated by cells and focus on the pivotal role of DNA repair and tolerance mechanisms in tumor resistance to cisplatin. In fact, several recent clinical findings have correlated the tumor cell status of DNA repair/translesion synthesis with patient response to cisplatin treatment. Furthermore, these mechanisms provide interesting targets for pharmacological modulation that can increase the efficiency of cisplatin chemotherapy." @default.
- W2897926526 created "2018-10-26" @default.
- W2897926526 creator A5002321293 @default.
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- W2897926526 creator A5059993172 @default.
- W2897926526 creator A5079483159 @default.
- W2897926526 date "2018-01-01" @default.
- W2897926526 modified "2023-10-01" @default.
- W2897926526 title "DNA repair pathways and cisplatin resistance: an intimate relationship" @default.
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