Presumably require facilitated opening in order for annealing to occur, leading the authors to speculate that Streptomyces species may require proteins to carry out the functions of Hfq. Consequently, the identification of such an RNA chaperone in Streptomyces could aid in the development of synthetic asRNAs since synthetic RNAs could then be designed to mimic naturally occurring trans-acting sRNAs. The use of peptide-PNAs in Streptomyces is of particular interest as genetic transformation is not required for gene silencing, thus they can be used in species in which genetic tools have not been established or to simply accelerate the process of genetic analysis. The current synthesis costs and high concentrations required when using these molecules in agar-based assays makes optimization studies prohibitive. However, improvements in micro-culture of Streptomyces and reduced synthesis costs will enable different peptide-PNA designs to be evaluated for this genus. In summary, recent reports reveal that Streptomyces use endogenous transcripts to regulate gene expression, and here we show for the first time that synthetic strategies using expressed RNA or a delivered DNA mimic can provide useful levels of RNA silencing. As a method, RNA silencing can be used to improve our understanding of Streptomyces biology and possibly alter metabolic flux in industrial applications. Gliomas are the most common primary brain tumors, accounting for 80% of malignant central nervous system neoplasms.Recent genome-wide mutational analysis has demonstrated that the incidence of IDH1 mutations in gliomas ranges from 5% in primary glioblastoma to 70% in anaplastic astrocytomas and 80% in secondary GBM. Patients with high-grade astrocytomas with IDH1 mutations were reported to have a better survival. The IDH1 gene is located on 2q33.3 and its mutation has been described in a very restricted number of human cancers including gliomas.The most common IDH1 mutation is a heterozygous missense mutation with a change of guanine to adenine at position 395, leading to the replacement of arginine by histidine at codon132 at the AbMole Niflumic acid enzymatic active site. IDH1 mutation has been shown to occur in early stage of gliomagenesis. The pathogenesis of IDH1-R132H-related tumorigenesis is rapidly being elucidated. Not only does loss of function occur with reduced production of a-ketoglutarate from isocitrate, the R132H mutation also confers a gain of function to the mutant IDH1, which 
converts a-KG to 2hydroxyglutarate. Accumulation of this oncometabolite induce sextensive DNA hypermethylation, leading to genomewide epigenetic changes and predisposing cells toward neoplastic transformation. In spite of all the studies, the role of IDH1 mutation in the recurrence of gliomas is unknown. There have been few studies in which paired gliomas at primary presentation and recurrence were studied by molecular means.