A central role for HER3 in HER2-amplified breast cancer: implications for targeted therapy.

By S. Lee-Hoeflich, Lisa M. Crocker, E. Yao, Thinh Q. Pham, Xander Munroe, K. Hoeflich, M. Sliwkowski, H. Stern. Cancer Research, 2008

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Ligand-independent HER2/HER3/PI3K complex is disrupted by trastuzumab and is effectively inhibited by the PI3K inhibitor GDC-0941. (2009, methodology): “We recently confirmed and extended upon these observations by using a combination of RNA silencing of HER receptor expression, a tumor model with inducible HER3 knockdown, and the analysis of HER3 activation status in HER2-positive breast cancer specimens (Lee-Hoeflich et al., 2008).”
Phase II study of the antibody drug conjugate trastuzumab-DM1 for the treatment of human epidermal growth factor receptor 2 (HER2)-positive breast cancer after prior HER2-directed therapy. (2011, background): “Pertuzumab is an HER2directed monoclonal antibody that blocks heterodimerization and ligand-dependent signaling of HER1/HER2 and HER2/HER3 heterodimers.(22) Pertuzumab in combination with trastuzumab demonstrated clinical activity (ORR, 24.”
Pertuzumab plus Trastuzumab plus Docetaxel for Metastatic Breast Cancer (2011, neutral): “HER2 has no ligand, and HER3 does not have tyrosine kinase activity.(16) Receptor dimerization is an essential requirement for HER function and can occur between two different HER members (heterodimerization) or between two molecules of the same receptor (homodimerization).”