Like cisplatin, it contains two chloride ligands, which are released within the cellular environment and interact with DNA to form intra- and interstrand cross-links.3 These DNA adducts trigger multiple cellular responses, including DNA damage recognition and repair, cell cycle arrest, and activation of apoptotic signaling pathways, ultimately inhibiting cell proliferation.4 Ovarian cancer remains one of the leading causes of mortality among gynecological malignancies, with epithelial ovarian carcinoma accounting for more than 90% of all cases.5 The current standard therapy involves primary cytoreductive surgery followed by platinum-based combination chemotherapy administered as soon as possible after surgery.6 However, a major limitation of these treatments is the dose-dependent toxicity associated with platinum compounds, which can result in significant off-target tissue injury.7 It is well established that Reactive Oxygen Species (ROS) generated during the metabolism of platinum-based agents contribute to this toxicity, particularly in the reproductive system
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Phosphorylation regulates cullin-based ubiquitination in tumorigenesis
Among these, random mutagenesis techniques such as ultraviolet (UV) irradiation effectively generate phenotypic diversity without using recombinant DNA technology (Jeyachandran et al., 2024)
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Results often begin within 4 weeks and last around 12 weeks, improving with continued cycles
