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EGFRs selectively activate AKT () and STAT (see ) signaling pathways, which promote cell survival, but have no effect on extracellular signal-regulated kinase signaling, which induces proliferation.

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Treatment with metformin in combination with gefitinib resulted in a more pronounced decrease in the levels of protein phosphorylation (p-MAPK, p-AKT).

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As confirmation of the effects of nuclear PKM2 on CRC cell apoptosis, gefitinib-induced apoptosis was analyzed in C2BBel cells transfected with the PKM2 shRNA vector, and the tumor cells transfected with nonspecific shRNA acted as controls.

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In a tumor with the 2240del18 mutation from a patient with nonsmall cell lung cancer who showed responsiveness to gefitinib with complete remission over a 2-year period, identified the development of a second mutation in EGFR, thr790 to met (T790M; ), responsible for secondary resistance to gefitinib.

EGFR mutation specific immunohistochemistry is a useful adjunct which helps to identify false negative mutation testing in lung cancer.

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We next examined colony formation in the presence of gefitinib alone or combined with metformin.

We found that ARMS could improve the mutation detection rate and the mutation positive patients responded well with TKIs therapy, but the correlation between mutation negative patients and TKIs therapy was still unsatisfactory.

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The study was supported by Research Fund for Capital Medical Development (2007-3042) and Beijing Municipal Natural Science Foundation (7112100).

Although no patients developed acute interstitial pneumonia, the possibility of drug-related interstitial lung disease could not be excluded because of the small number of patients in our series.

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Six of the 25 patients (24%) with gefitinib-related ILD required invasive mechanical ventilation and all patients were treated with steroids.

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No resulta claro si la diferencia de resultados en estos dos estudios, fue producto de las diferencias en la población estudiada, la caracterización del tumor en la expresión EGFR o regímenes quimioterapéuticos.

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However, the compelling results we have achieved on the synergistic antiproliferative effect together with the fold of dose reduction obtained in combination setting for both gefitinib and IFN-α compared with each drug alone, both in vitro and in vivo, indicate a direct and effective cross-talk between EGFR-mediated and IFN-α-induced pathways that need to be further investigated.

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