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. 2011 Oct 21;16(11):1535–1546. doi: 10.1634/theoncologist.2011-0165

Table 2.

Summary of mechanisms of trastuzumab resistance

graphic file with name onc01111-0901-t02.jpg

Respective roles in intrinsic and acquired resistance based on current evidence, their prevalence in HER-2–overexpressing breast cancer, and alternative targeting strategies and agents to overcome trastuzumab resistance are also shown.

Abbreviations: EGFR, epidermal growth factor receptor; HER, human epidermal growth factor receptor; HSP90, heat shock protein 90; IGF-1R, insulin-like growth factor 1 receptor; mTOR, mammalian target of rapamycin; mTORC, mTOR complex; PI3K, phosphoinositide 3-kinase; PTEN, phosphatase and tensin homologue deleted on chromosome ten; RTK, receptor tyrosine kinase; T-DM1, trastuzumab-DM1 conjugate.