Trastuzumab-induced HER2 phosphorylation: exploring the mechanisms and implications

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Targeting of ErbB family of receptor tyrosine kinases (RTKs) is frequently used to inhibit the oncogenic signaling in different malignancies. Lapatinib, a dual selective tyrosine kinase inhibitor (TKI) of EGFR and HER2, inhibits their tyrosine kinase activities and receptor tyrosine phosphorylation. Cetuximab, a chimeric monoclonal antibody (mAb) directed against the extracellular domain of EGFR, prevents EGF-mediated receptor kinase activation and tyrosine phosphorylation. However, trastuzumab, a humanized mAb directed against HER2, induces EGFR and HER2 receptor tyrosine phosphorylation and this agonistic effect is correlated with its inhibition of cancer cell proliferation. This review will focus on the current understanding of molecular mechanisms and implications of trastuzumab-induced tyrosine phosphorylation of HER2.

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