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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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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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Secondary end-points were overall survival (OS), objective response rate (ORR), health-related quality of life (HRQoL), symptom improvement, safety and tolerability.
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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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Currently, the question of whether or not to test a diagnostic specimen in early-stage disease is a local decision that must be made in conjunction with each institution's oncology care team, as insufficient published evidence supports a universal recommendation.
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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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