The genotoxic drug doxorubicin (Dox) remains one of the most powerful chemotherapeutic options available for a wide range of cancers including breast, ovarian, and other cancers. However, emerging evidence links Dox treatment with chemotherapy-induced cognitive impairment, a condition that is popularly referred to as Dox-induced neurotoxicity or “chemobrain”, which limits the use of the drug. There are no specific treatments for Dox-induced neurotoxicity, only interventions to mitigate the neurotoxic effects of the drug. Accumulating evidence indicates that DNA damage, oxidative stress, dysregulation of autophagy and neurogenesis, inflammation, and apoptosis play central roles in Dox-induced neurotoxicity. Additionally, germline mutations in the tumour suppressor genes breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) increase the risk of breast, ovarian, and related cancers. BRCA1 and BRCA2 are distinct proteins that play crucial, unique roles in homologous recombination-mediated double-stranded break repair. Furthermore, BRCA1 and 2 mitigate oxidative stress in both neural cells and brain microvascular endothelial cells, which suggests that they have a critical role as regulators of pathways central to the development of Dox-induced neurotoxicity. Despite research on the effects of Dox on cognitive function, there is a gap in knowledge about the role of BRCA1 and BRCA2 in Dox-induced neurotoxicity. In this review, we discuss existing findings about the role of different mechanisms and the role of BRCA1 and BRCA2 in Dox-induced neurotoxicity, along with future perspectives.

Cancer is highly prevalent disease and one of the leading causes of global morbidity and mortality, however, about 50% of all cancer cases can be prevented through healthy living and policies that protect health. Stress, which has become an integral part of modern lifestyles, is considered as a hallmark of cancer. Chronic stress-related maladaptive response, immunosuppression, and inflammation – all directly increase the risk for the cancer development. Chronic stress also indirectly contributes by promoting unhealthy behaviours, such as overeating, smoking, drinking and hormonal imbalance – all of which induce inflammation promoting cancer development. Inflammation is also caused by many other factors, such as bacterial and viral infections, autoimmune diseases, and chemical exposure. This review is about stress and lifestyle-related behaviors and mechanisms that increase the risk for developing different types of cancer, and policies and strategies to educate people in early ages to take mindful decisions which can prevent the development of cancer in time.