The structures were elucidated on the basis of NMR spectroscopic and mass spectrometry data. Compounds 1-4 exhibited antimalarial and cytotoxic activities. (C) 2011 Phytochemical Society of Europe. Published by Elsevier B.V. All rights reserved.”
“OBJECTIVE: Available chemotherapy presents poor control over the development of metastatic melanoma.

FTY720 is a compound already approved by the Food and Drug Administration for the treatment of patients with multiple sclerosis. It has also been observed that FTY720 inhibits tumor growth in vivo (experimental models) and in vitro (animal and human tumor cells). The aim of this study was to evaluate the effects of FTY720 on a metastatic melanoma model and in tumor cell lines.

METHODS: We analyzed FTY720 efficacy selleck BVD-523 inhibitor in vivo in a syngeneic murine metastatic melanoma model, in which we injected tumor cells intravenously into C57BL/ 6 mice and then treated the mice orally with the compound for 7 days. We also treated mice and human tumor cell lines with FTY720 in vitro,

and cell viability and death pathways were analyzed.

RESULTS: FTY720 treatment limited metastatic melanoma growth in vivo and promoted a dose-dependent decrease in the viability of murine and human tumor cells in vitro. Melanoma cells treated with FTY720 exhibited characteristics of programmed cell death, reactive oxygen species generation, and increased beta-catenin expression. In addition, FTY720 treatment resulted in an

immunomodulatory effect in vivo by decreasing the percentage I-BET-762 price of Foxp3+ cells, without interfering with CD8+ T cells or lymphocyte-producing interferon-gamma.

CONCLUSION: Further studies are needed using FTY720 as a monotherapy or in combined therapy, as different types of cancer cells would require a variety of signaling pathways to be extinguished.”
“Spinocerebellar ataxias (SCAs) constitute a heterogeneous group of more than 30 autosomal-dominant genetic and neurodegenerative disorders. SCAs are generally characterized by progressive ataxia and cerebellar atrophy. Although all SCA patients present with the phenotypic overlap of cerebellar atrophy and ataxia, 17 different gene loci have so far been implicated as culprits in these SCAs. It is not currently understood how mutations in these 17 proteins lead to the cerebellar atrophy and ataxia. Several pathogenic mechanisms have been studied in SCAs but there is yet to be a promising target for successful treatment of SCAs. Emerging research suggests that a fundamental cellular signaling pathway is disrupted by a majority of these mutated genes, which could explain the characteristic death of Purkinje cells, cerebellar atrophy, and ataxia that occur in many SCAs.