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NSCLC reported that EGFR activating mutations were the most important independent predictors for time to treatment failure compared with other mutations, among which exon 19 deletion and L858R mutations were the best predictors for longer time to treatment failure in a multivariate analysis ().

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Proteins that are normally produced in very low quantities but whose production is dramatically increased in tumor cells, trigger an immune response.

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The role of chemotherapy prior to surgery in patients with stage III N2 NSCLC has been extensively tested in clinical trials.

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PPL conceived of the study, participated in its design and coordination, and helped to draft the manuscript.

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Similar results have been obtained using gefitinib, an EGFR tyrosine kinase inhibitor (TKI; refs.

Hepatocellular carcinoma (HCC) is a molecular complex tumor with high intrinsic drug resistance.

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High EGFR copy number predicts benefits from tyrosine kinase inhibitor treatment for non-small cell lung cancer patients with wild-type EGFR.

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Doi T, Koizumi W, Siena S, Cascinu S, Ohtsu M, Michael H, Takiuchi H, Swaisland N, Gallagher E, Cutsem V (2003) Efficacy, tolerability and pharmacokinetics of gefitinib (ZD1839) in pretreated patients with metastatic gastric cancer.

Co-overexpression of fibroblast growth factor 3 and epidermal growth factor receptor is correlated with the development of nonsmall cell lung carcinoma.

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Whilst impressive clinical benefits have been observed for NSCLC with a known driver mutation, acquired resistance is frequently seen and presents us with the next challenge in the goal to deliver unique personalised medicine.

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