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Boswellic acid formulations are not suitable for additive treatment of pediatric high-grade glioma

ABSTRACT: Boswellic acid formulations are not suitable for additive treatment of pediatric high-grade glioma

PROVIDER: PRJNA887686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21822740.fastq.gz	Fastqsanger.gz
	SRR21822741.fastq.gz	Fastqsanger.gz
	SRR21822742.fastq.gz	Fastqsanger.gz
	SRR21822743.fastq.gz	Fastqsanger.gz
	SRR21822744.fastq.gz	Fastqsanger.gz

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Boswellic acid formulations are not suitable for additive treatment of pediatric high-grade glioma

Project description:Introduction: Pediatric high-grade gliomas (pedHGG) comprise a very poor prognosis. Thus, parents of affected children are increasingly resorting to complementary and alternative medicine (CAM). Among others, one of the most frequently used CAM are boswellic acids (BA). Methods: The therapeutic effectiveness of the three main BA, alpha-boswellic acid (α-BA), beta-boswellic acid (β-BA) and 3-acetyl-11-keto-beta-boswellic acid (AKBA) was analyzed in a histone 3 (H3)-wildtype and a H3.3K27M-mutant pedHGG cell line, either alone or in combination with radiotherapy and/or temozolomide chemotherapy. Cell viability, stemness properties and apoptosis as well as mRNA sequencing and in ovo tumor growth was investigated upon BA treatment. Results: Whereas α-BA and β-BA exert only mild anti-tumor effects in H3WT and H3.3K27M-mutated pedHGG cells, AKBA treatment reduced cell viability and stemness potential especially in H3.3K27M-mutant pedHGG cells. In addition, slight anti-inflammatory effects were observed after AKBA treatment of H3.3K27M-mutant pedHGG cells. However, no effects on apoptosis and in ovo tumor growth were found. Of note, α-BA and β-BA treatment even resulted in tumor promoting effects in both pedHGG cells.

2023-08-15 | GSE214897 | GEO

Boswellic acid formulations are not suitable for treatment of pediatric high-grade glioma due to tumor promoting potential

Project description: Not available

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Project description:The grade of pancreatic neuroendocrine tumors principally influences therapy. Grading is currently done by the histological examination of biopsy samples, which is an invasive and time-consuming method. We performed an NGS on FFPE tumor tissue samples to find microRNAs that show a significant difference in expression according to grade, thus could be suitable for grade determination.

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Project description:Expression profiling analyses for 5 maize inbreds and 4 hybrids, chosen to represent diversity in genotypes and heterosis responses, revealed a correlation between genetic diversity and transcriptional variation. The majority of differentially expressed genes in each of the different hybrids exhibited additive expression patterns, and ~25% exhibited statistically significant non-additive expression profiles. Among the non-additive profiles, ~80% exhibited hybrid expression levels between the parental levels, ~20% exhibited hybrid expression levels at the parental levels and ~1% exhibited hybrid levels outside the parental range. These findings indicate that the frequencies of additive and non-additive expression patterns are very similar across a range of hybrid lines. Keywords: Genotype comparison series

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Project description:Diffuse gliomas represent the most prevalent class of primary brain tumor. Despite significant recent advances in the understanding of glioblastoma (WHO IV), its most malignant subtype, lower-grade (WHO II and III) glioma variants remain comparatively understudied, especially in light of their notably variable clinical behavior. To examine the foundations of this heterogeneity, we performed multidimensional molecular profiling, including global transcriptional analysis, on 101 lower-grade diffuse astrocytic gliomas collected at our own institution, and validated our findings using publically available gene expression and copy number data from large independent patient cohorts. We found that IDH mutational status delineated molecularly and clinically distinct glioma subsets, with IDH mutant (IDH mt) tumors exhibiting TP53 mutations, PDGFRA overexpression, and prolonged survival, and IDH wild-type (IDH wt) tumors exhibiting EGFR amplification, PTEN loss, and unfavorable disease outcome. Furthermore, global expression profiling revealed three robust molecular subclasses within lower-grade diffuse astrocytic gliomas, two of which were predominantly IDH mt and one almost entirely IDH wt. IDH mt subclasses were distinguished from each other on the basis of TP53 mutations, DNA copy number abnormalities, and links to distinct stages of neurogenesis in the subventricular zone (SVZ). This latter finding implicates discrete pools of neuroglial progenitors as cells of origin for the different subclasses of IDH mt tumors. In summary, we have elucidated molecularly distinct subclasses of lower-grade diffuse astrocytic glioma that dictate clinical behavior and demonstrate fundamental associations with both IDH mutational status and neuroglial developmental stage. 80 tumor samples, one normal tissue sample (brain)

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Project description:High-grade glioma is highly aggressive and malignant, resistant to combined therapies and easy to relapse. A better understanding of circRNA biological function in high-grade glioma might contribute to the therapeutic efficacy. Here, a circRNA merely up-regulated in high-grade glioma, circGLIS3 (hsa_circ_0002874, originating from exon 2 of GLIS3), was validated by microarray and qRT-PCR. Functional experiments uncovered that up-regulation of circGLIS3 promoted glioma cell migration and invasion, and showed aggressive characteristics in tumor-bearing mice. Fluorescence in situ hybridization, RNA pull-down, RNA immunoprecipitation and immunohistochemical staining showed that circGLIS3 could promoted Ezrin T567 phosphorylation. Further investigation showed that circGLIS3 could be excreted by glioma through exosomes and induced endothelial cells angiogenesis. This study indicates that circGLIS3 is up-regulated in high-grade glioma and contributes to the invasion and angiogenesis of glioma via promoting Ezrin T567 phosphorylation.

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