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Anthracycline cardiotoxicity mechanisms remain incompletely defined; leaves open targeted prevention strategies in survivors.
Despite advancements in oncological treatments, anthracyclines still form the basis of the treatment. Anthracycline chemotherapy plays a prominent role in treating many forms of cancer. Unfortunately, the dose-dependent and cumulative cardiotoxicity limit the use of anthracyclines. 1 Cardiotoxic side effects limit their dosing, and improved cancer outcomes expose the cancer survivor to increased cardiovascular morbidity and mortality. The exact mechanism of anthracycline-induced cardiotoxicity is still unclear, al-though it is likely to be multifactorial. The primary mechanism of cardiotoxicity may involve direct pathways for reactive oxygen species generation and topoisomerase II, and other indirect pathways. Application of various strategies can minimize anthracycline-induced cardiotoxicity; one such method is dexrazoxane, a cardioprotective agent. Dexrazoxane has been used in cancer patients to prevent anthracycline-related cardiotoxicity since the 1980s. Dexrazoxane, an ethylene diamine tetraacetic acid, such as Evaluation of Demographic Parameters, Disease Burden, and Cardiovascular
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DENİZ et al. (2021) studied this question.
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