Fluoxetine Counteracts the Cognitive and Cellular Effects of 5-Fluorouracil in the Rat Hippocampus by a Mechanism of Prevention Rather than Recovery

5-Fluorouracil (5-FU) is a cytostatic drug associated with chemotherapy-induced cognitive impairments that many cancer patients experience after treatment. Previous work in rodents has shown that 5-FU reduces hippocampal cell proliferation, a possible mechanism for the observed cognitive impairment, and that both effects can be reversed by co-administration of the antidepressant, fluoxetine. In the present study we investigate the optimum time for administration of fluoxetine to reverse or prevent the cognitive and cellular effects of 5-FU

Cardiovascular and Central Nervous System Toxicity by Anticancer Drugs in Breast Cancer Patients

Breast cancer is one of the most malignant diseases, associated with high rate mortality. In this chapter a particular attention is paid on cardiovascular and central nervous system toxicity induced by chemotherapeutic agents used for both primary and metastatic treatment of this life-threatening pathology. With respect to traditional drugs, including anthracyclines, taxanes, and fluoropyrimidines, the more recent targeted therapies, such as human epidermal growth factor receptor 2 (HER2) and vascular endothelial growth factor (VEGF), aimed to ameliorate anticancer activity and to reduce toxic effects by affecting more specific molecular sites. However, despite the improvement in breast cancer treatment, these novel drugs were also found to be associated, even if at a lesser extent, with important side effects, such as cardiotoxicity, with consequent heart failure. For this reason, the cardiovascular and brain safety profile of all anticancer drugs and protocols remains important items to be carefully evaluated in breast cancer patients