Modifiers on the absorption Aurora kinases of dasatinib administration of a single dose of ranitidine at least 4 h after administration of dasatinib in all patients. We observed minimal antitumor activity Th Including Highest probably due to the phase I design, the degree of the patient prior to treatment Lich prior bevacizumab therapy in more than 50%, and all exhibits low dasatinib. Limited anti-tumor was recently reported for dasatinib and erlotinib in patients with NSCLC. M Possible strategies to improve the antitumor activity of t of this system in the CNS tumor future studies erh Hen k Can dasatinib twice t Possible, and the inclusion of an enriched population of patients who will likely benefit from EGFR inhibitors and SFK. In addition, the assessment of patients less heavily pretreated and those not progressed on bevacizumab can addict Write the anti-tumor benefits. Closing Lich’s efforts to assess the impact of concurrent gastric pH modifiers on exposure of dasatinib to minimize particularly relevant for patients with malignant glioma. Conclusion We report the first clinical study with built-in combination therapy targeting EGFR and SFK in patients with malignant glioma. Best addition to the establishment of maximum tolerated dose We term that can be the targets of the EGFR and SFK be performed safely in patients with malignant glioma. Although the combination therapy against mediators interactive cellular Re signaling pathways activated faulty signaling an attractive therapeutic approach for many complex cancers, including normal malignant glioma, a sorgf insurance valid assessment of pharmacokinetic and pharmacodynamic interactions for assessing the inhibition of the target, and the identification of a subgroup of patients with an increased Hten probability of response is enhanced, will likely be necessary, addictive to the success of this approach. Dasatinib is a dual SRC-family kinase / Abl inhibitor, which is about 300 times more potent than imatinib in inhibiting the tyrosine kinase BCR-ABL in vitro. Dasatinib binds to ABL requirements less stringent than that informational imatinib BCR stim match, making it less anf Llig for resistance mutations in BCR-ABL kinase. The efficacy of dasatinib on the front line was reported in a Phase 2 study to MDACC. As seen in nilotinib, dasatinib was high CCyR and MMR, the associated occurred at the beginning of treatment. A second phase 2 trial, the Intergroup trial S0325, was carried out by four groups of North American cooperation. It was a randomized comparison of dasatinib 100 mg / d compared ima tinib 400 mg / d, the prime Re endpoint was a 4-log reduction of BCR ABL transcript in 12 months. Both treatments were very effective and had anything similar progression-free survival rates and free operating system. Remarkably, Dasatinib induces low-molecular reactions to 10 months, but not much more than 4 log reduction in BCR-ABL compared to imatinib. A high number of missing samples showed the early nature of these data, the data in the L Be ngerfristig. Phase 3, randomized dasatinib vs. imatinib in patients with newly diagnosed CML-CP study investigated treatment with dasatinib 100 mg / d compared with imatinib 400 mg / day in patients with newly diagnosed CML-CP. Dasatinib showed significant h Here rates of CCR and MMR tinib at 12 months compared to ima. Zus Tzlich is an h Herer proportion of patients with such responsibility.