Nitiate malignant transformation, or to the erismodegib sensitivity of tumors to erlotinib or HKI to provide 272 short-term treatment. As highlighted in in vitro studies, the presence of other ErbB family members affect the effectiveness of the inhibition of EGFR. Further studies are needed to determine the r Of the ErbB2 and ErbB3 in our mouse model in lung tumorigenesis and the m Different reactions resembled the kinase-Dom Ne mutations hEGFR twelve fifty-eight long-term treatment of EGFR inhibition. EGFR targeted therapies in lung tumors with overexpression of mutated hEGFR kinase Dom mice ne are very effective at M, With clinical observations in humans that most NSCLC patients with mutations in the kinase-Dom Ne hEGFR the answer erlotinib or gefitinib or the other. Our mouse model data suggest that lung tumors caused by mutations in the kinase-Dom Ne hEGFR dependent Ngig of the activated EGFR to survive and thus a biological explanation Caused tion for the marked tumor responses through the inhibition of this pathway . However, mutations in the EGFR kinase Cathedral Ne, which is only 10% of lung adenocarcinomas in Caucasians and 30% of East Asian patients. It also seems to be NSCLC patients with EGFR Weight clinical benefit from gefitinib and erlotinib therapy with stable disease and prevent further progression. In vitro studies have suggested that weight can not play hEGFR expression in NSCLC an r The leading role in the malignant transformation or survival pathways, but happy in the way t the spread of weapons of mass destruction to be involved in cell. In line with these in vitro observations to date we have not succeeded in observing the development of lung tumors in the two founders with the overexpression of weight in the compartments of the lung hEGFR after 26 weeks of doxycycline. It is m Possible that lung tumors with a latency time was much l singer and / or other genetic Ver Changes with p53 or PTEN simultaneous development of these Mice overexpressing EGFR wt of lung cancer is required. HKI 272 is an irreversible inhibitor which covalently binds to the EGFR kinase Cathedral Ne of the slit, w During erlotinib and gefitinib are reversible EGFR inhibitors.
Almost all patients with NSCLC tumors harbor Kinasedom Ne mutations hEGFR first response gefitinib or erlotinib, but closing Lich develop resistance to these inhibitors. Molecular analyzes of tumors have relapsed showed secondary one T790M mutation re hEGFR. HKI is in vitro capable of 272 to overcome this resistance. Recently we have also shown that HKI 272 is effectively dependent in the treatment of lung tumors Ngig of EGFRvIII M Nozzles, EGFRvIII, an EGFR mutation and thereby the activation Rahmengeh Mice a deletion of exon 2-7, was found that in a small percentage of human squam se lung cancer. Here we show that HKI 272 is entered as effective as erlotinib in the treatment of tumors Born by the expression of two main groups hEGFR kinase Dom ne mutants. It w re Interesting to determine the effectiveness of HKI 272 in comparison to erlotinib and gefitinib in patients who were not exposed to EGFR inhibitors and to determine whether a different spectrum of resistance mutations would after chronic treatment with either class of EGFR to develop inhibitors or in combination. Our results with the treatment with cetuximab in lung cancer M Mice entered Born by EXP.