Insulin-like growth factor-I receptor signaling and resistance to trastuzumab (Herceptin).

By Yuhong Lu, X. Zi, Yunhua Zhao, D. Mascarenhas, Michael Pollak. Journal of the National Cancer Institute, 2001

937 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/36556ed69c30e239396afbeaa6a03f9156654d5e

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In Molecular Biology

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Citations in the corpus

• Insulin receptor isoforms and insulin receptor/insulin-like growth factor receptor hybrids in physiology and disease. (2009, background): “One mechanism may involve increased IGF-IR signaling, as described for breast cancer cells resistant to the anti-HER2/ErbB2 monoclonal antibody, trastuzumab (286), and for colorectal cancer cells resistant to antiEGFR monoclonal antibody 225 (287).”
• Targeting HER2-positive breast cancer with trastuzumab-DM1, an antibody-cytotoxic drug conjugate. (2008, background): “... proportion of patients treated with trastuzumab either do not respond initially or relapse after experiencing a period of clinical response (5, 9). Progression through trastuzumab-containing therapy is attributed to aberrant activation of signaling pathways, such as the phosphatidylinositol 3-ki”
• PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients. (2004, methodology): “implicated in trastuzumab resistance, but it has not been validated with clinical data (Lu et al., 2001).”
• ErbB receptors and signaling pathways in cancer. (2009, background): “In another study activation of the insulin-like growth factor-1 receptor (IGF-IR) in ErbB2+ breast cell lines renders initially trastuzumab-sensitive cells resistant to the antibody [53], and this was linked to PI3K/Akt activation [54].”
• Trastuzumab: mechanism of action, resistance and future perspectives in HER2-overexpressing breast cancer. (2007, background): “[38] engineered the human breast cancer cell line SKBR3 to overexpress IGF-IR in order to assess the efficacy of trastuzumab.”
• Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “In addition, activation of HER-related receptors, such as HER3, or non-HER receptors, such as insulin-like growth factor I receptor, have been suggested in preclinical studies to increase PI3K/AKT signaling thereby limiting trastuzumab efficacy (Lu et al., 2001; Sergina et al., 2007).”