Cardiac side effects of trastuzumab: lessons learned from targeting cancer pathways

Debu Tripathy

This article has no abstract so we have provided the first paragraph of the full text.

Unexpected toxicity from agents that target cancer-related pathways will become a more familiar theme as we are ushered into the era when these agents outnumber standard chemotherapeutic drugs. The signaling networks of carcinogenesis, growth, development and metabolism are interrelated and complex, with clinical effects that are difficult to predict. It has long been recognized that deregulation of developmental genes can be carcinogenic as a result of the inappropriate recapitulation of the phenotype of embryonic cell migration and invasion of tissue boundaries. During the latter phases of the pivotal randomized trials of the HER2-oncogene-directed antibody trastuzumab it became apparent that cardiomyopathy was an uncommon treatment-related complication, which was more pronounced in those receiving concurrent cardiotoxic anthracycline therapy.¹ At about the same time, findings of the HER2 knockout mouse were reported, showing impairment of the development of cardiac trabeculae and cranial neural-crest-derived sensory ganglia.² More recent studies have shown that cardiac myocyte-targeted HER2 gene knockout in adult mice leads to impaired cardiac remodeling in response to stress.³

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