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Serious adverse reactions were reported in 29% of patients treated with afatinib.

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Interestingly, overexpression of wild-type FOXM1 or constitutively active FOXM1 did not efficiently overcome the antiproliferative effect of gefitinib, indicating that gefitinib may either have other cell cycle regulators as targets or also regulate FOXM1 activity through other post-transcriptional mechanisms.

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Engelman JA, Jänne PA, Mermel C, Pearlberg J, Mukohara T, Fleet C, Cichowski K, Johnson BE, Cantley LC: ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines.

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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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The observation that certain subgroups of patients, particularly female patients, those who have never smoked, those who have adenocarcinoma histology, and those who are of Asian descent, have a higher response rate and clinical benefit with gefitinib and erlotinib therapy prompted research to elucidate the molecular mechanism responsible for this increased response.

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Seven (15 %) of these had also received further palliative systemic therapy (including platins, 5-fluorouracil, taxanes and triapine (a novel ribonucleotide reductase inhibitor)) prior to commencing gefitinib.

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Our work also underscores the need to consider incorporating repeated biopsies into clinical studies of novel targeted therapies, such as those involving mutant tyrosine kinases.

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Although both drugs also phosphorylated eIF2α in PC-9 cells, which are human lung cancer cell line and are extremely sensitive to EGFR inhibitors, the protective effect of TUDCA was not found in this cell line ( and Figs), suggesting that TUDCA treatment would not disturb the anti-cancer efficacy of EGFR inhibitors in non-small cell lung cancer patients.

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