Ubsequent tests recently tissue P-glycoprotein for molecular analysis is also important because previous treatment of the relevant genotypes modify VER Can. In our patients treated with EGFR-TKI in 33 biopsies of tissues in recent years, one of which had eight of the T790M genotype. Unfortunately, none of the patients responded T790M, perhaps due to inadequate dosage. In future studies examine strategies for the treatment of acquired resistance to EGFR-TKI, all patients should ideally have developed a tissue analysis for resistance to the interaction of treatment with the Molecular Biology of the plaintiff tion TKIresistant disease. Development of non-invasive tests, such strategies will facilitate the circulating tumor cells based on this process. In addition to the observation that mutations in exons 19 L Mixtures significantly h More frequently in our cohort were that L858R, extremely low frequency of EGFR FISH-positive patients in the cohort of wild-type EGFR compared to the rates generally in the range 30% of reported notable.34 Although several studies have suggested that the gene copy number by FISH is a useful alternative biomarker for selecting patients Secretase Signalingfor EGFR-TKI first-generation, recent studies comparing chemotherapy with TKI n ‘have not supports this Out.4, 24.34 38 argued the low H FREQUENCY of positive fish among wild-type patients in our study, be that FISH-positive patients are not suitable for long-term survivors after TKI treatment, if the small arm B limits the power of this observation. Other biomarkers may be of interest, but not here, as MET and HER2 analyzes. Other dual-TKI EGFR/HER2 were disappointed; Traded in NSCLC, but none was sorgf Validly up to date in patients who previously received EGFR-TKI studied the first generation, and many are still in the development of TT. Lapatinib, a reversible inhibitor of pan ErbB, was very successful in HER2-positive breast cancer, but had minimal activity t in NSCLC.39 41 CI 1033, an irreversible inhibitor of ErbB pan has not reached its preset end in a phase II study XL647 in NSCLC unselected patients.42 Newer agents such as double PF00299804 inhibitorsBIBW2992 irreversible and reversible inhibitor, are still under active study in populations with NSCLC mutations selected by just increments of EGFR-TKI response before the first generation to have the status of the KRAS wild-type or clinical characteristics, but the results of these tests are not yet available. Because lapatinib, neratinib has recently completed a major activity t of HER2-positive breast cancer.43 presented summary, we showed that neratinib, an irreversible inhibitor of pan ErbB binding, has little clinical activity T 240mgdaily previously in patients with NSCLC will benefit you of EGFR-TKI first-generation TKIs in patients with adenocarcinoma ï naive and smoking habits or very few. Significant and sustained responses were observed in the small cohort of patients with mutations in the EGFR G719X. Future studies in NSCLC with neratinib will focus on trying, the dose Diosmetin and / or plan to reduce diarrhea and obtain h Higher doses biological processes Change. Activity of t observed. Of the 25 patients were treated with breast cancer who were evaluable tumor responses in phase I trial, eight patients had a partial remission, all of these players had had back U prior treatment with trastuzumab.