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. 2010 May 1;16(9):2489-95.
doi: 10.1158/1078-0432.CCR-09-2318. Epub 2010 Apr 20.

New strategies in head and neck cancer: understanding resistance to epidermal growth factor receptor inhibitors

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New strategies in head and neck cancer: understanding resistance to epidermal growth factor receptor inhibitors

Lucy F Chen et al. Clin Cancer Res. .

Abstract

The epidermal growth factor receptor (EGFR) is a validated target in squamous cell carcinoma of the head and neck (HNSCC). However, despite high expression of EGFR in these cancers, EGFR inhibitor monotherapy has only had modest activity. Potential mechanisms of resistance to EGFR-targeted therapies involve EGFR and Ras mutations, epithelial-mesenchymal transition, and activation of alternative and downstream pathways. Strategies to optimize EGFR-targeted therapy in head and neck cancer involve not only the selection for patients most likely to benefit but also the use of combination therapies to target the network of pathways involved in tumor growth, invasion, angiogenesis, and metastasis.

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Figures

Figure 1
Figure 1
EGFR Signaling Pathway and Several Mechanisms of Resistance to EGFR-Targeted Therapies Abbreviations: EGFR: epidermal growth factor receptor K-Ras: v-KI-RAS2 Kirsten rat sarcoma viral oncogene homolog H-Ras: v-Ha-ras Harvey rat sarcoma viral oncogene homolog PTEN: phosphatidylinositol phosphatase mTOR: mammalian target of rapamycin mAbs: monoclonal antibodies TKIs: tyrosine kinase inhibitors

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