A positive pr Diktiver The study was conducted on the hypothesis that inhibition of COX LOX 2 or 5, the effectiveness buy ADX-47273 of platinum-based chemotherapy in advanced NSCLC can improve k. Researchers have attempted to inhibit both paths, the AA metabolites has been shown to regulate angiogenesis, apoptosis resistance and invasion and metastasis. Patients with NSCLC IIIB or IV 2 PS0 has once again U carboplatin AUC 5.5, gemcitabine 1000 mg/m2 and 600 mg po qid zileutin, CG celecoxib 400 mg po bid or CGZ celecoxib. Endpoints included PFS and OS. The study did not meet its set target of a 50% PFS 9 months. In correlative studies have shown that COX-2 IHC survive a negative prognostic factor for this, but a positive pr Diktiver factor for survival is if patients have again U celecoxib.
Einhorn et al. J Thorac Oncol MGCD-265 page 14 Author manuscript, increases available in PMC 13th June 2012. Multivariate Analysis best Preferential interaction of COX-2 expression and response to celecoxib. A Phase III study tests the hypothesis that inhibition of COX-2 is beneficial in patients with tumors overexpressing COX-2 is discussed. Target in a second paper on the treatment to the combination of AA pathway, said Dr. Karen Reckamp Phase I study of erlotinib combination with celecoxib. The activated overexpression of COX-2 extracellular Re signal-regulated kinase / mitogen-activated protein kinase signaling pathway in a manner against EGFR-TKI. The overexpression of COX-2 also inhibits tumor E-cadherin expression in dependence Dependence prostaglanding E2.
This is important because low E-cadherin expression was associated with resistance to EGFR-TKI. Because pr Clinical data showed that tumor COX-2 expression caused resistance to EGFR-TKI, to determine a phase I study of optimal biological dose, defined as the maximum decrease in urinary prostaglandin EM and toxicity profile t of combination of celecoxib and erlotinib carried out in the NSCLC. Twenty-two patients with stage IIIB / IV NSCLC were new U increasing doses of celecoxib 200 to 800 mg twice t And resembled a fixed dose of erlotinib. Prim Re endpoints were to assess the toxicity of t and the determination of the OBD of celecoxib to erlotinib. Secondary Re endpoints examined exploratory biomarkers and clinical response.
Twenty-two patients were recruited, and 21 were evaluable for the determination of the OBD, toxicity t and response. Effects and toxicity of skin rash Th were the most hours Ufigsten reported and in 86% of patients. There was no DLT and no cardio-toxicity T be studied in connection with the treatment. All subjects were evaluated on the intention to treat. Seven patients showed a partial response and five patients had stable disease develops. Responses were observed in patients with activating EGFR mutations. A significant decline in urinary PGE-M was after 8 weeks of treatment, and the OBD of celecoxib 600 mg twice t Shown possible. This study defines the OBD of celecoxib with a fixed dose of EGFR TKI. These results demonstrate objective responses with acceptable side effect profile. Future studies with COX inhibition with two strategies, the OBD of celecoxib 600 mg twice t Possible. A randomized phase II study in patients with advanced NPC