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- Tavina L. Offutt; Pek U. Ieong; Özlem Demir; Rommie E. Amaro
- Biochemistry 2018 v.57 no.46 pp. 6528-6537
- DNA; DNA damage; DNA-binding domains; apoptosis; asymmetry; cell cycle checkpoints; crystal structure; drug resistance; genome; genomics; humans; hypoxia; models; molecular dynamics; mutants; neoplasms; site-directed mutagenesis; transcription factors; transcriptional activation
- ... The “guardian of the genome”, p53, functions as a tumor suppressor that responds to cell stressors such as DNA damage, hypoxia, and tumor formation by inducing cell-cycle arrest, senescence, or apoptosis. Mutation of p53 disrupts its tumor suppressor function, leading to various types of human cancers. One particular mutant, R175H, is a structural mutant that inactivates the DNA damage response pa ...
- Bapurao Surnar; Nagesh Kolishetti; Uttara Basu; Anis Ahmad; Erik Goka; Brian Marples; David Kolb; Marc E. Lippman; Shanta Dhar
- Biochemistry 2018 v.57 no.46 pp. 6500-6513
- DNA; DNA damage; adverse effects; antineoplastic activity; aspirin; cisplatin; drug therapy; in vitro studies; models; nausea; nephrotoxicity; neurotoxicity; patients; urinary bladder neoplasms
- ... Cisplatin is a major chemotherapeutic that continues to have a significant impact in the treatment of more than 50% of all cancers. Since its Food and Drug Administration approval in 1978 for the treatment of advanced ovarian and bladder cancer, this chemotherapeutic has made significant strides and its application has been extended to a large variety of other cancers. However, the vast majority o ...