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Basic research | Clinical research |
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(1) Exploration beyond the oxidative stress hypothesis as a primary mechanism of anthracycline cardiotoxicity | (1) Reduction of anthracycline cardiotoxicity in clinical practice |
(2) Implementation of long-term studies in animal models | (2) Identification of early signs of cardiac damage |
(3) Identification of predictive markers of cardiac damage | (3) Educate clinicians: anthracycline-induced cardiotoxicity can initially respond to cardiac medications |
(4) Determination of the relative impact of different mechanisms of myocardial damage | (4) Determination of the cardiotoxicity of targeted and combination therapies |
(5) Exploration into the relationship between growth factors and anthracyclines | (5) Identification of a balance between cardiotoxicity with clinical benefit |
(6) Understanding drug interactions in new combination therapies | (6) Definition of risks and benefits for subgroups of patients |
(7) Assessment of the effects of anthracyclines on cardiac development | (7) Management of cardiac dysfunction in cancer survivors treated with anthracyclines |
(8) Assessment of the effects of anthracyclines on non-myocyte cardiac cells | (8) Specifications of dietary and exercise recommendations for anthracycline-treated patients |
(9) Assessment of risk-benefit factors in groups with compounding risk factors for cardiomyopathy | (9) Understanding the progression of anthracycline cardiomyopathy: systolic versus diastolic heart dysfunction |
(10) Determination of genetic predispositions to anthracycline cardiotoxicity | (10) Expansion of the use of dexrazoxane and liposomal anthracyclines |
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