Ean kitf III and directly with Big 5-HT Receptor Dye Terminator v1.1 sequencing kitg sequences of the primers and lacing on an ABI Prism 3130 sequencer.h mutations were observed systematically reviewed in a new reverse transcription reaction. This method could detect the mutant allele, when in 5-10% of the cells to pr Sentieren. The analysis of statistical differences dog and tumor characteristics were T-test for continuous variables and Pearson analyzesW2 or Fisher exact tests for categorical variables. Outcome measures Ma Were were using the product limit method, and the curves generated by the Kaplan-Meier method. The dogs were stratified by tumor characteristics and differences in the actuarial Sch Estimates were tested by the log-rank method. In this study, dogs were censored in the analysis were, as she lost to follow-up was the death was not caused by MCT or treatment, or relapse had not occurred before the end of the study period. Differences were considered significant at Po.05. Statistical analysis was performed using SAS 9.1.i Results Patient characteristics between February 2005 and October 2006, 202 dogs for response and toxicity t of treatment evaluated with masitinib. Detailed characteristics of dogs are shown in Table 1. The h Ufigsten breeds were Labrador Retrievers, Golden Retrievers, Boxers and. Dogs get a first-line treatment with masitinib of 42.1% of Bev Lkerung of the test, and had composed the remaining 57.9% again U medical treatment for MCT. Had the majority of dogs included in the study inoperable tumors, and the remainder had tumors that were recurrent after surgery. The diagnosis was made months before the start of the O12 Masitinib treatment in most dogs. Furthermore, had the most dogs with grade II MCTs, and the rest of grade III tumors. The properties of the MCT and dogs were not significantly different between the arms masitinib and placebo in the study. KIT mutation status in tumor biopsies by reverse transcription PCR was determined for 191 of the 202 dogs and is described in detail elsewhere.10 under masitinib treated dogs had described, 26.7%, a mutation in the KIT and KIT mutations was 25.6% with placebo-treated dogs found. Of the 50 dogs with mutations had the most mutations in the juxtamembrane Cathedral sharing plans. Mutations were also h Frequently found in exons 8 and 9, and one dog had a mutation in exon 17th These mutations all appear to constitutive activation of the kinase domain.10 The proportion of dogs with mutant forms of KIT did not differ significantly between the masitinib and placebo arm, causing the study. Engaged efficacy in the treatment of dogs with MCT masitinib TTP masitinib significantly compared with placebo in all dogs agrees on. This effect was more pronounced Gter if the dog again U masitinib as first-line treatment, and the first-line treatment with masitinib erh Ht fa TTP is significant independently Ngig of whether the tumors are a form of the type expressed mutant or wild-type KIT. In addition to dogs with a mutated form of KIT masitinib as second-line treatment or sp Ter had to l Ngere TTP compared with placebo, but the difference was not statistically significant due to the small number of dogs in this subgroup. within 14 days. An analysis of these dogs do not identify the presence of.
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