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[Cancer Research 62, 200-207, January 1, 2002]
© 2002 American Association for Cancer Research

Experimental Therapeutics

Insulin-like Growth Factor Receptor I Mediates Resistance to Anti-Epidermal Growth Factor Receptor Therapy in Primary Human Glioblastoma Cells through Continued Activation of Phosphoinositide 3-Kinase Signaling1

Arnab Chakravarti2, Jay S. Loeffler and Nicholas J. Dyson

Departments of Radiation Oncology [A. C., J. S. L.] and Molecular Oncology [N. J. D.], Massachusetts General Hospital/Harvard Medical School, Charlestown, Massachusetts 02129

Overexpression of the epidermal growth factor receptor (EGFR) has been shown previously to correlate with enhanced malignant potential of many human tumor types, including glioblastoma multiforme (GBM). Anti-EGFR targeting has been demonstrated to enhance apoptosis and reduce both cellular invasion and angiogenic potential. It remains unclear whether absolute EGFR expression levels are sufficient to predict which tumors will respond best to anti-EGFR therapy. We have identified two primary GBM cell lines with equivalent EGFR expression levels with very different sensitivities to the EGFR receptor tyrosine kinase inhibitor, AG1478. This was apparent despite similar reductions in EGFR signaling in both cell lines, as measured by phospho-EGFR levels. AG1478 enhanced both spontaneous and radiation-induced apoptosis and reduced invasive potential in the GBMS, but not in the GBMR, cell line. The resistant GBMR cell line demonstrated an up-regulation of insulin-like growth factor receptor I (IGFR-I) levels on AG1478 administration. This resulted in sustained signaling through the phosphoinositide 3-kinase pathway, resulting in potent antiapoptotic and proinvasion effects. Cotargeting IGFR-I with EGFR greatly enhanced both spontaneous and radiation-induced apoptosis of the GBMR cells and reduced their invasive potential. Akt1 and p70s6k appeared to be important downstream targets of IGFR-I-mediated resistance to anti-EGFR targeting. These findings suggest that IGFR-I signaling through phosphoinositide 3-kinase may represent a novel and potentially important mechanism of resistance to anti-EGFR therapy.




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C. L. Arteaga and J. Baselga
Clinical Trial Design and End Points for Epidermal Growth Factor Receptor-targeted Therapies: Implications for Drug Development and Practice
Clin. Cancer Res., May 1, 2003; 9(5): 1579 - 1589.
[Full Text] [PDF]

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 Cancer Res.Home page
D. Sachdev, S.-L. Li, J. S. Hartell, Y. Fujita-Yamaguchi, J. S. Miller, and D. Yee
A Chimeric Humanized Single-Chain Antibody against the Type I Insulin-like Growth Factor (IGF) Receptor Renders Breast Cancer Cells Refractory to the Mitogenic Effects of IGF-I
Cancer Res., February 1, 2003; 63(3): 627 - 635.
[Abstract] [Full Text] [PDF]

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 J. Biol. Chem.Home page
A. Hurbin, L. Dubrez, J.-L. Coll, and M.-C. Favrot
Inhibition of Apoptosis by Amphiregulin via an Insulin-like Growth Factor-1 Receptor-dependent Pathway in Non-small Cell Lung Cancer Cell Lines
J. Biol. Chem., December 13, 2002; 277(51): 49127 - 49133.
[Abstract] [Full Text] [PDF]


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