Particulate radiation-induced gliomas
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA540964 | ENA |
REPOSITORIES: ENA
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Project description:Trangenic mice with brain-targeted deletion of one allele of p53 and one allele ot Pten were irradiated with particulate radiation. Radiation induced gliomas were analyzed to identify copy number variations
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Project description:Long-term complications such as radiation-induced second malignancies occur in a subset of patients following radiation-therapy, particularly relevant in pediatric patients due to the long follow-up period in case of survival. Radiation-induced gliomas (RIGs) have been reported in patients after treatment with cranial irradiation for various primary malignancies such as acute lymphoblastic leukemia (ALL) and medulloblastoma (MB). We perform comprehensive (epi-) genetic and expression profiling of RIGs arising after cranial irradiation for MB (n=23) and ALL (n=9). Our study reveals a unifying molecular signature for the majority of RIGs, with recurrent PDGFRA amplification and loss of CDKN2A/B and an absence of somatic hotspot mutations in genes encoding histone 3 variants or IDH1/2, uncovering diagnostic markers and potentially actionable targets.
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Project description:Radiation-induced gliomas represent H3-/IDH-wild type pediatric gliomas with recurrent PDGFRA amplification and loss of CDKN2A/B.
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Project description:Long-term complications such as radiation-induced second malignancies occur in a subset of patients following radiation-therapy, particularly relevant in pediatric patients due to the long follow-up period in case of survival. Radiation-induced gliomas (RIGs) have been reported in patients after treatment with cranial irradiation for various primary malignancies such as acute lymphoblastic leukemia (ALL) and medulloblastoma (MB). We perform comprehensive (epi-) genetic and expression profiling of RIGs arising after cranial irradiation for MB (n=23) and ALL (n=9). Our study reveals a unifying molecular signature for the majority of RIGs, with recurrent PDGFRA amplification and loss of CDKN2A/B and an absence of somatic hotspot mutations in genes encoding histone 3 variants or IDH1/2, uncovering diagnostic markers and potentially actionable targets.
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Project description:The goal of this study was to compare the radiation-induced gene translation profiles generated from human tumor cell lines that are treated with radiation. Keywords: stimulus or stress design A panel of cell lines included 5 gliomas, 4 pancreatic carcinomas, 3 breast carcinomas and 2 non-small cell lung carcinomas. In addition, radiation-induced gene translation profiles were generated for 4 normal human cell lines: a skin fibroblast (BJ), 2 lung fibroblasts (MRC5, MRC9) and mammary epithelial (MEC). Specifically, cell lines were exposed to 2 Gy or sham irradiated, polysome-bound RNA was isolated 6h later and subjected to microarray analyses. Each cell line was evaluated in biological replicates.
2010-07-20 | E-GEOD-10547 | biostudies-arrayexpress
Project description:Long-term complications such as radiation-induced second malignancies occur in a subset of patient following radiation-therapy, particularly relevant in pediatric patients due to the long follow-up period in case of survival. Radiation-induced gliomas (RIGs) have been reported in patients after treatment with cranial irradiation for various primary malignancies such as acute lymphoblastic leukemia (ALL) and medulloblastoma (MB). Our study revealed a unifying molecular signature for the majority of RIGs, with recurrent PDGFRA amplification and loss of CDKN2A/B and an absence of somatic hotspot mutations in genes encoding histone 3 variants or IDH1/2, uncovering diagnostic markers and potentially actionable targets.
2019-12-24 | GSE131482 | GEO
Project description:Purpose: Determine the mechanism of particulate matter-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with particulate matter (5 μg/cm2) and incubated for 24 h. Total RNA (1 ug) from melanocytes were extracted and subjected to library synthesis. Results: Particulate matter-treated melanocytes exhibited upregulation of ER stress, unfolded protein response, and melanogenesis-related molecules. Conclusion: Particulate matter-induced melanocyte signaling was well evaluated using RNA sequencing.
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Project description:Gene Expression Profile of Radiation Therapy Resistant BRAFV600E Pediatric Gliomas
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Project description:Inhibitors of the MAPK pathway (MAPKi) have shown significant activity in treatment of childhood BRAF-activated brain tumors. However, for tumors harboring BRAFV600E mutations, the drugs are rarely curative, and patients can become refractory to treatment. Combining MAPKi with low dose X-ray therapy (XRT) has the potential to improve the cure rate, but development of XRT resistance poses a major challenge. To understand the mechanisms of radiation resistance in BRAFV600E type pediatric low-grade gliomas, radiation resistance models were developed by using BT-40 pediatric low-grade glioma (PLGG) PDX model harboring BRAFV600E mutation. RNA sequencing was performed to determine the gene expression profile of primary tumors and resistant tumors. Each tumor tissue was transplanted to 3 scid mice respectively. When tumor volume reach ~0.3~0.6 cm3, tumor tissue (from three mice, triplicates) were collected and were snap-frozen in liquid nitrogen. RNA was isolated and applied to subsequent 100bp paired read sequencing run with Illumina NovaSeq 6000 platform at 100 bp paired-end module.
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Project description:Glioblastoma (GBM) is the most aggressive brain tumor and resistant to current available therapeutics, such as radiation. To improve the clinical efficacy, it is important to understand the cellular mechanisms underlying tumor responses to radiation. Here, we investigated long-term cellular responses of human GBM cells to ionizing radiation. Comparing to the initial response within 12 hours, gene expression modulation at 7 days after radiation is markedly different. While genes related to cell cycle arrest and DNA damage responses are mostly modulated at the initial stage; immune-related genes are specifically affected as the long-term effect. This later response is associated with increased cellular senescence and inhibition of transcriptional coactivator with PDZ-binding motif (TAZ). Mechanistically, TAZ inhibition does not depend on the canonical Hippo pathway, but relies on enhanced degradation mediated by the β-catenin destruction complex in the Wnt pathway. We further showed that depletion of TAZ by RNAi promotes radiation-induced senescence and growth arrest. Pharmacological activation of the β-catenin destruction complex is able to promote radiation-induced TAZ inhibition and growth arrest in these tumor cells. The correlation between senescence and reduced expression of YAP as well as β-catenin also occurs in human gliomas treated by radiation. Collectively, these findings suggested that inhibition of TAZ is involved in radiation-induced senescence and might benefit GBM radiotherapy.
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