Insulin-like growth factor-I receptor/human epidermal growth factor receptor 2 heterodimerization contributes to trastuzumab resistance of breast cancer cells.

By R. Nahta, L. Yuan, Bing Zhang, R. Kobayashi, F. Esteva. Cancer Research, 2005

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How researchers see this paper

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Mechanisms of Disease: understanding resistance to HER2-targeted therapy in human breast cancer (2006, background): “We recently demonstrated that crosstalk occurs between IGF1R and HER2, and showed that IGF1R physically interacts with and induces phosphorylation of HER2 in trastuzumab-resistant cells, but not in trastuzumab-sensitive parental cells”
ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “Indeed, modulation of levels of p27 appears to be a common endpoint for several of the resistance pathways noted above, including signaling from IGF-1R and MET (Nahta et al., 2005; Shattuck et al., 2008).”
Human Epidermal Growth Factor Receptor 2 (HER2) in Cancers: Overexpression and Therapeutic Implications (2014, neutral): “HER2 can also be activated by complexing with other membrane receptors such as insulin-like growth factor receptor 1 [12].”
Treatment of HER2-positive breast cancer: current status and future perspectives (2012, background): “activates the PI3K/Akt pathway and this mechanism is thought to be an important source of trastuzumab resistance”
Targeting HER2-positive breast cancer with trastuzumab-DM1, an antibody-cytotoxic drug conjugate. (2008, background): “At present, available data indicate that cancer cells do not lose HER2 expression when they become refractory to HER2-directed therapies (14, 16).”