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. 2022 Oct 6;12:1006429. doi: 10.3389/fonc.2022.1006429

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Copyright © 2022 Wang, Zheng, Jia, Liu, Xiao, Chen, Liang and Lu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Molecular mechanisms of trastuzumab resistance in HER2-positive breast cancer. These molecular mutations mainly impact cell signaling and proliferation, leading to trastuzumab resistance. Alterations of HER2 influencing downstream pathways abate the pharmacologic effect of trastuzumab. A truncated form of HER2 called p95-HER2 lacks the extracellular domain that binds trastuzumab and is related with poor response to trastuzumab. d16-HER2, derived from exon 16 skipping in ERBB2, generates activated d16-HER2 homodimers on the tumor cell surface to activate SRC kinase, resulting in cell proliferation and tumorigenesis.