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The IC50 of gemcitabine in resistant cells cocultured with 5 μM of gefitinib was significantly decreased from 290.

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However, no studies have investigated the efficacy of gefitinib dose-escalation in these SD patients after one month of standard gefitinib dosage.

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We examined the in vitro cell growth inhibition of gefitinib or MTE on NSCLC cells by using MTT assay.

Combination approaches may be significantly more effective than single treatments.

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Thus, these clones exhibit, on average, 10-fold increased resistance to HKI-272, but 100-fold more resistance to gefitinib and erlotinib.

Already, new treatments targeting genetic alterations in other, less common driver oncogenes are being evaluated in lung cancer, and testing for these may be addressed in future versions of these guidelines.

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In fact, the ECOG analysis focused on patients above the age of 70 years and noted higher degree of toxicity with bevacizumab-based treatment, while the AVAiL and SAIL analyses used a cut-off age of 65 years and did not report any unexpected safety signals.

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In fact, on the basis of the structural similarity between ABL and EGFR tyrosine kinases, the T790M change has been introduced into wild-type EGFR; this altered EGFR has high-level resistance to anilinoquinazoline inhibitors.

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The type of genomic information generated by TCGA and other cancer genomics projects will drive research to develop similar treatment strategies that will be most effective for a given set of genomic changes.

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Other class II activating mutations result in a glycine-719 (G719) change to serine, alanine or cysteine (4% of all EGFR TK activating mutations), and other missense mutations account for another 6% of EGFR mutations.

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