Resistance to EGFR-TKI can be mediated through multiple signaling pathways converging upon cap-dependent translation in EGFR-wild type NSCLC.

Abstract excerpt

INTRODUCTION: For the majority of patients with non-small-cell lung cancer (NSCLC), response to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is suboptimal. In models of acquired resistance to EGFR-TKI, activation of Akt phosphorylation is frequently observed. Because Akt activation results in downstream initiation of cap-dependent protein translation, we hypothesized that a strategy of...

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