A Systematic Review of the Cardiotoxic Effects of Targeted Therapies in Oncology.

Cancer therapy advancements have improved survival rates but also introduced significant cardiotoxic risks. Cardiotoxicity, a critical adverse effect of cancer treatments such as doxorubicin, trastuzumab, and radiotherapy, poses substantial challenges. This systematic review synthesizes findings from studies on cardiotoxicity induced by cancer therapies, focusing on detection and management. Key predictors of chemotherapy-induced myocardial toxicity (CIMT) include advanced age, hypertension, hyperlipidemia, diabetes, and elevated N-terminal pro-B-type natriuretic peptide levels. Regular echocardiographic assessments, particularly of the left ventricular global longitudinal strain (LVGLS) and left ventricular ejection fraction (LVEF), are essential for early detection. The CardTox-Score, incorporating these risk factors, shows high sensitivity and specificity in predicting CIMT. Advanced imaging techniques and biomarkers play crucial roles in identifying at-risk patients before functional decline. Early biomarkers and imaging techniques such as LVGLS and LVEF are effective in diagnosing and managing cardiotoxicity, allowing timely interventions. Cardiology involvement in patient care significantly enhances adherence to cardiac monitoring guidelines and reduces cardiotoxicity risks. Management strategies emphasize regular cardiac monitoring, patient education, and the use of cardioprotective agents. A collaborative approach between cardiologists and oncologists is vital to assess cardiovascular risks, minimize vascular toxicity, and manage long-term adverse effects, ensuring the safety and efficacy of cancer therapies. This review underscores the importance of early detection and proactive management of cardiotoxicity in cancer patients to optimize treatment outcomes and improve quality of life.

Cytotoxicity of Quantum Dots in Receptor-Mediated Endocytic and Pinocytic Pathways in Yeast.

Despite the promising applications of the use of quantum dots (QDs) in the biomedical field, the long-lasting effects of QDs on the cell remain poorly understood. To comprehend the mechanisms underlying the toxic effects of QDs in yeast, we characterized defects associated with receptor-mediated endocytosis (RME) as well as pinocytosis using Saccharomyces cerevisiae as a model in the presence of cadmium selenide/zinc sulfide (CdSe/ZnS) QDs. Our findings revealed that QDs led to an inefficient RME at the early, intermediate, and late stages of endocytic patch maturation at the endocytic site, with the prolonged lifespan of GFP fused yeast fimbrin (Sac6-GFP), a late marker of endocytosis. The transit of FM1-43, a lipophilic dye from the plasma membrane to the vacuole, was severely retarded in the presence of QDs. Finally, QDs caused an accumulation of monomeric red fluorescent protein fused carbamoyl phosphate synthetase 1 (mRFP-Cps1), a vacuolar lumen marker in the vacuole. In summary, the present study provides novel insights into the possible impact of CdSe/ZnS QDs on the endocytic machinery, enabling a deeper comprehension of QD toxicity.

The Impact of Cadmium Selenide Zinc Sulfide Quantum Dots on the Proteomic Profile of Saccharomyces cerevisiae.

Quantum dots (QDs) have been highly sought after in the past few decades for their potential to be used in many biomedical applications. However, QDs' cytotoxicity is still a major concern that limits the incorporation of QDs into cutting-edge technologies. Thus, it is important to study and understand the mechanism by which QDs exert their toxicity. Although many studies have explored the cytotoxicity of quantum dots through the transcriptomic level and reactive species generation, the impact of quantum dots on the expression of cellular protein remains unclear. Using Saccharomyces cerevisiae as a model organism, we studied the effect of cadmium selenide zinc sulfide quantum dots (CdSe/ZnS QDs) on the proteomic profile of budding yeast cells. We found a total of 280 differentially expressed proteins after 6 h of CdSe/ZnS QDs treatment. Among these, 187 proteins were upregulated, and 93 proteins were downregulated. The majority of upregulated proteins were found to be associated with transcription/RNA processing, intracellular trafficking, and ribosome biogenesis. On the other hand, many of the downregulated proteins are associated with cellular metabolic pathways and mitochondrial components. Through this study, the cytotoxicity of CdSe/ZnS QDs on the proteomic level was revealed, providing a more well-rounded knowledge of QDs' toxicity.