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We have been told that these agents are extremely selective for one tyrosine kinase, but I think that these drugs do many things, and when the cells die, it is not because the EGFR is blocked.

Companies can then do a genetic screening of known SNPs sprinkled across the genomes of the individuals tested to see whether the subpopulation has a SNP or multiple SNPs that are not present in the genetics of the other individuals.

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Moreover, hematologic toxicity was confined to patients treated with vinorelbine.

Multitargeted Tyrosine Kinase Inhibitor: Results of a Phase II Study in Subjects with Non-small Cell Lung Cancer Who Have Progressed after Responding to Treatment with Either Gefitinib or Erlotinib.

We pretreated the cells with SU11274 for 48 h before adding, for the final 4 h, the PKC δ inhibitor rottlerin, GO6976 (an inhibitor blocking the activities of classical PKCs only), or CI-1033 (an irreversible ErbB TKI).

Exposure to sunlight increases the risk that you will develop a rash during your treatment with erlotinib.

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Moreover, we have shown recently that EGF has a protective effect on IFN-α-induced apoptosis that is targeted on the stress pathway terminal kinases (), suggesting that EGFR signaling suppresses apoptosis behaving like a survival pathway.

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One explanation for this discrepancy is that once patients in the chemotherapy arm experience disease progression, they can still display high RRs and prolonged PFS after switching to an EGFR TKI.

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For these patients, timely diagnosis is critical and molecular testing should be initiated as soon as a diagnosis of adenocarcinoma is established.

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