U0126 is significantly smaller Wnt Pathway than the mean tumor volume in mice M, Re U vehicles, OSI 906 alone or U0126 alone. Immunohistochemical F Staining for Ki67 and caspase 3 in tumors have shown that the combined treatment, a decrease in cell proliferation in conjunction with increased Hter induced cell apoptosis in vivo. Taken together, these results underscore the R The central activation of the MEK / ERK-K-Ras mutation in the primary R-resistance of NSCLC cells to IGF-1R ITC. Discussion In this study, we developed potential pr Diktiven markers of response of NSCLC cells to IGF-1R ITC. We show that: 1 The expression of IGF 1R/IR in NSCLC samples were positive with a history of smoking, squamous, WT EGFR and KRAS mutant, two somatic mutations of EGFR, which gives dependence connected dependence of EGFR signaling channel, induces a prime re response to the absence of IGF 1R TKI in NSCLC cells, and 3 K-ras mutation causes increased hte production of IGF-1 and the way the activation of the IGF 1R, but induces resistance to IGF 1R ITC. In addition, our results provide a proof of principle that targeted inactivation of the IGF 1R by a TKI, in combination with inhibition of MEK, a favorable outcome in the treatment of NSCLC patients are given with a history of smoking and K-Ras mutant. Several pr Clinical and clinical studies have shown encouraging therapeutic efficacy of EGFR TKIs in NSCLC with mutated EGFR2, 3, however, emphasize the limited response to the EGFR TKI need effective treatment strategies for patients with WT EGFR todevelop. Narrow path IGF 1R is a new strategy. The two main Ans Tze are small molecules TKIs and IGF 1R monoclonal anti-IGF 1R. However, only limited data on the Pr Predictors of sensitivity to anti-Ans Tze IGF 1R. In this study we have determined predictors Pr Used in clinical trials with IGF 1R TKIs in patients with NSCLC k nnten. Previous studies have demonstrated high Ma IGF-1R expression in carcinomas in Epidemo Histology.27 shown by the analysis of a TMA sample of 354 patients with NSCLC, we extended this observation and shows a high Ma of PlGF 1R / IR in patients with carcinoma Epidemo of. These data suggest that squamous cell k can More sensitive to IGF 1R TKI that adenocarcinoma of the lung. However, previous reports and show our current results suggest that tumor histology is not a pr Diktiver marker of response to IGF 1R targeted strategies. We also observed markedly Here 1R/IR PlGF in patients with a history of smoking, those with mutant KRAS, and EGFR with WT, all with very poor response to EGFR TKI-associated merchandise. Numerous studies have suggested that human cancer cells can k Highly Ma E of single or multiple pathways that are activated and a tumorigenic potential, 28 and 30 successful cancer treatment strategies in the selection of patients with tumors that it depends lengths, these paths are based on cell growth and survival. Our results show that past and current lines transformed lung epithelial cells caused by components of tobacco had high expression of PlGF 1R/IR and were sensitive to targeted strategies against the IGF 1R molecular system.