Abstract
Trastuzumab represents the predominant therapy to target breast cancer subtype marked by HER2 amplification. It has been in use for two decades and its continued importance is underlined by recent FDA approvals of its biosimilar and conjugated versions. Progression to an aggressive disease with acquisition of resistance to trastuzumab remains a major clinical concern. In addition to a number of cellular signaling pathways being investigated, focus in recent years has also shifted to epigenetic and non-coding RNA basis of acquired resistance against trastuzumab. This article provides a succinct discussion on the most recent advances in our understanding of such factors.
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