Comparatively,

numerous other strategies, both those involving cellular transplantation and those examining neutralisation of inhibitory factors of the CNS, have achieved limited success. A combinational strategy, with olfactory ensheathing selleck kinase inhibitor cells at its centre, is arguably the best way forward in encouraging effective recovery following CNS injury.

This review examines the inhibitory environment of the CNS and the research to date on overcoming its effects on the regrowth of injured axons. The efficacy of therapies involving olfactory ensheathing cells, and the place of these therapies among the many other strategies being developed is examined. (c) 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Background Cabazitaxel

is a novel tubulin-binding taxane drug with antitumour activity in docetaxel-resistant cancers. We aimed to compare the efficacy and safety of cabazitaxel plus prednisone with those of mitoxantrone plus prednisone in men with metastatic castration-resistant prostate cancer with progressive disease after docetaxel-based treatment.

Methods We undertook an open-label randomised phase 3 trial in men with metastatic castration-resistant prostate cancer who had received previous hormone therapy, but whose disease had progressed during or after treatment with a docetaxel-containing regimen. Participants were treated with 10 mg oral prednisone daily, and were randomly assigned to receive either 12 mg/m(2) mitoxantrone intravenously find more over 15-30 min or 25 mg/m(2) cabazitaxel intravenously over 1 h every 3 weeks. The random allocation schedule was computer-generated; patients and treating physicians were not masked to treatment allocation, but the study team was masked to the data analysis. The primary endpoint was overall survival. Secondary endpoints included progression-free survival and safety. Analysis was by intention to treat. This study is registered at ClinicalTrials.gov, NCT00417079.

Findings 755 men were allocated to treatment groups (377 mitoxantrone, 378 cabazitaxel) and were included in the

intention-to-treat analysis. At the cutoff for the final analysis (Sept 25, 2009), median survival was 15.1 months (95% CI 14.1-16.3) Blasticidin S ic50 in the cabazitaxel group and 12.7 months (11.6-13.7) in the mitoxantrone group. The hazard ratio for death of men treated with cabazitaxel compared with those taking mitoxantrone was 0.70 (95% CI 0.59-0.83, p<0.0001). Median progression-free survival was 2.8 months (95% CI 2.4-3.0) in the cabazitaxel group and 1.4 months (1.4-1.7) in the mitoxantrone group (HR 0.74, 0.64-0.86, p<0.0001). The most common clinically significant grade 3 or higher adverse events were neutropenia (cabazitaxel, 303 [82%] patients vs mitoxantrone, 215 [58%]) and diarrhoea (23 [6%] vs one [<1%]).