Dependence Independent activation. Cyclopamine, an antagonist, smoothed TTET has activity T pr against SCLC Clinical. Other smoothed Tteten antagonists can be developed k. In Similar way are antiques Body against the hedgehog ligands for new therapeutic agents directly analogous to monoclonal antibodies Body is directed against VEGF, buy ABT-888 which bekannterma S are considered in the treatment of lung cancer successfully. Of the hedgehog signaling pathway is probably important in maintaining stem cell lung cancer. Thus, the therapy directed against this path likely target the tumor stem cells. Telomerase inhibitors. Telomerase activity is t enabled in all lung cancers k Can all histological types.
This enzyme and its cofactor RNA are absolutely necessary for the growth of tumor cells immortal and the maintenance of telomere ends of chromosomes. W During normal stem cells in your body also express telomerase, have pr Clinical trials showed that there is a big e therapeutic window of telomerase in tumor cells inhibited without Sch Ending of the organism as a TG100-115 whole. GRN153L on telomerase RNA inhibitor component was developed and is effective in inhibiting telomerase. Extensive pr Clinical studies have found a significant activity T made against lung cancer xenografts of the test. He entered Phase I clinical studies and phase II trials in lung cancer are con Us. The key to their development is to integrate it with standard chemotherapy. Press show Clinical xenograft models of lung cancer, it m Is possible. Src inhibitors.
C-src family is a non-associated cytoplasmic tyrosine kinase signaling links growth factor, cytokine and integrin receptors on their cell surface Chemical signaling pathways downstream, such as effector PI3K/PTEN/Akt, statistics, Ras / Raf / ERK and focal adhesion kinase. The L Solution of this important metabolic pathways for SRC contr L growth and survival cell proliferation, invasion and metastasis, and angiogenesis. In lung cancer, may c Src with the EGFR and Src activity t may be necessary together for transformation by the EGFR. C. Src TKI currently in clinical trials go Ren dasatinib, AZD 0530, SKI and 606th The effects of dasatinib in NSCLC cells is dependent Ngig of cell-line, and conclude an arrest of cell cycle, apoptosis, and decreased cellular Ren invasion.
EGFR in cell lines or dependence ngigkeitsstatus diktiv is pr Mutant EGFR cell apoptosis, w while the cells of the wild-type EGFR dependent ngig to undergo EGFR proliferation stops are G1. Combination of the results of dasatinib and erlotinib in the synergistic inhibition of cell proliferation in cell lines sensitive to EGFR TKI. In Phase I trials with dasatinib, contain big e toxicity Gastrointestinal toxicity th t, fatigue and rash. A phase I / II study evaluating the safety and reps Possibility of erlotinib in previously treated dasatinib in patients with NSCLC in good condition and without prior exposure to EGFR TKI to test is already scheduled. AZD 0530 was in a phase I trial in solid tumors at doses ranging from 60 to 250 mg / day po for 14 days tested. DLT included febrile neutropenia and fatigue, and the maximum tolerated Possible dose was 175 mg / d Phase II trials are planned or in NSCLC, prostate cancer, melanoma, colon cancer and pancreatic cancer. Dubinett Steven Einhorn et al. Page 13 J Thorac