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Clinicians and patients were not masked to treatment allocation; independent review of tumour response was done in a blinded manner.

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PFS and OS were estimated using Kaplan-Meier methodology.

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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.

For patients whose tumors have activating mutations of EGFR, the dramatic responses to gefitinib of patients whose disease has been refractory to all other therapies suggest that this agent may be more effective if used earlier in the course of treatment.

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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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In untreated NSCLC, c-Met amplification occurs in 3% cases, but is seen in up to 22% of EGFR mutant tumors with acquired resistance to EGFR TKIs.

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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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