Why the study?
What are the mechanisms by which trastuzumab affects vascular homeostasis and leads to cardiotoxicity in breast cancer patients?
What are the mechanisms by which trastuzumab affects vascular homeostasis and leads to cardiotoxicity in breast cancer patients?
This review highlights the need to understand the mechanisms of trastuzumab-induced cardiotoxicity, particularly its effects on vascular homeostasis and endothelial dysfunction, to improve cardiovascular safety in breast cancer treatment.
May inform cardiac surveillance during trastuzumab therapy; leaves open targeted vascular interventions pending prospective validation.
Breast cancer is the most common cancer in the UK. Advances in the methods of early diagnosis as well as newer and more effective treatments have led to improvements of disease-free and overall survival over the last decade. Almost one-third of breast cancers present with an aggressive form characterized by increased expression of human epidermal growth receptor 2 (HER2) proteins. A targeted treatment using monoclonal antibodies against HER2 expression such as trastuzumab has been shown to improve survival. Unfortunately, there is a degree of cardiotoxicity associated with these agents, as inhibition of HER2 pathways can also impair cardioprotective pathways. In the present review, we discuss the mechanisms by which trastuzumab might affect vascular homeostasis leading to endothelial dysfunction. We also provide suggestions for future research examining the effects of trastuzumab on the vasculature in breast cancer.
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Sandoo et al. (2015) studied this question.
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