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Multimodal integration of transcriptomics, proteomics and radiomics improves prediction of recurrence in patients with IDH-mutant Glioma

ABSTRACT: Multimodal integration of transcriptomics, proteomics and radiomics improves prediction of recurrence in patients with IDH-mutant Glioma

PROVIDER: PRJNA939698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24072200_1.fastq.gz	Fastqsanger.gz
	SRR24072200_2.fastq.gz	Fastqsanger.gz
	SRR24072201_1.fastq.gz	Fastqsanger.gz
	SRR24072201_2.fastq.gz	Fastqsanger.gz
	SRR24072202_1.fastq.gz	Fastqsanger.gz

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Multimodal integration of transcriptomics, proteomics and radiomics improves prediction of recurrence in patients with IDH-mutant Glioma

Project description:Isocitrate dehydrogenase mutant gliomas remain lethal brain cancers which impair quality of life in young adults. These tumors are molecularly and cellularly heterogeneous and have a wide range of survival prognoses. Consequently, the identification of pa Here, we analyzed imaging, transcriptomic, and proteomic profiles using machine learning to 1) describe the biological characterization of subtypes of IDH-mutant gliomas categorized by PET and histology, 2) reinforce the integration of PET metrics in the

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Radiomics Predicts High or Low Recurrence Risk and is Associated with LncRNAs in Breast Cancer

Project description:The key radiomic features were found to vary after neoadjuvant chemotherapy. Moreover, lncRNAs were discovered to be significantly correlated with radiomics and recurrence-free survival (RFS). The findings indicate that the radiomic signature can be conveniently used for individualized prediction of RFS and that radiomics is associated with lncRNAs in breast cancer.

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Project description:This dataset is the proteomics part of a multi-parametric integration of transcriptomics, proteomics and radiomics with clinical data using machine learning in patients with IDHmutant Glioma.Our integrative analysis provides a better stratification of IDH-mutant gliomas patients and their risk of recurrence, which will lead to a better monitoring of the clinical evolution of the disease.

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Heterogenous radiomics patterns are associated with poor survivals and dysregulated pathways in medulloblastoma

Project description:Background. To develop a radiomics signature for predicting overall survival (OS) and progression-free survival (PFS) in patients with medulloblastoma (MB), and to investigate the incremental prognostic value and underlying biological pathways of the radiomics signature.Methods. A radiomics signature was constructed based on five magnetic resonance (MR) sequences (T1, T1c, T2, FLAIR and ADC) from a training cohort (n = 83) using LASSO-Cox model. Association between the signature and survival was evaluated on a testing cohort (n = 83). Incremental prognostic value of the signature beyond clinicomolecular factors was assessed with respect to calibration, discrimination, reclassification and clinical usefulness by a radiomics-clinicomolecular nomogram. Key pathways associated with the signature were identified. Prognostic value of pathway genes was assessed in a public TCGA cohort.Results. The radiomics signature was significantly associated with OS/PFS, independent from clinicomolecular factors. The radiomics-clinicomolecular nomogram predicted OS (C-index 0.762) and PFS (C-index 0.697) better than either the radiomics signature (C-index: OS: 0.649; PFS: 0.593) or the clinicomolecular nomogram (C-index: OS: 0.725; PFS: 0.691) only, with a better calibration and classification accuracy (net reclassification improvement: OS: 0.298, P = 0.022; PFS: 0.252, P = 0.026). Nine pathways were significantly correlated with the radiomics signature. Average expression value of pathway genes achieved significant risk stratification in public cohort (log-rank P = 0.016). Conclusion. This study demonstrated radiomics signature was an independent prognostic marker and offered incremental value over clinicomolecular factors in OS/PFS predictions for MB patients. The signature was associated with dysregulated pathways affecting patient prognosis in MB.

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Genotyping by array of 297 adult-type diffuse gliomas comprise IDH-mutant astrocytomas, IDH-mutant 1p/19q codeleted oligodendrogliomas, and IDH-wildtype glioblastomas

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2014-10-03 | E-GEOD-62008 | biostudies-arrayexpress

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Project description:Genome-wide DNA methylation profiling of 226 longitudinally collected IDH-wildtype glioblastoma tumor specimens from 106 patients, consisting of 99 initial treatment-naive resection specimens prior to any radiation or chemotherapy and 127 recurrent post-treatment resection specimens at time of recurrence/progression usually following radiation and/or chemotherapy. These 127 recurrent post-treatment resection specimens were composed of 106 first surgically-treated recurrent specimens, 19 second surgically-treated recurrent specimens, and 2 third surgically-treated recurrent specimens. The Illumina Infinium EPIC 850k version 1.0 Human DNA Methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpG sites of genomic DNA extracted from formalin-fixed, paraffin-embedded tumor tissue of the 226 IDH-wildtype glioblastomas.

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Project description:IDH mutant cells are deficient in retinoic acid production, which impacts downstream gene expression and pathways. We looked at the effect of supplementing IDH mutant glioma cells with ATRA on gene expression and downstream pathways. We compared gene expression changes with IDH WT cells that were also treated with ATRA

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Insulator dysfunction and oncogene activation in IDH mutant gliomas

Project description:Gain-of-function IDH mutations define major clinical and prognostic classes of gliomas. Mutant IDH protein produces a novel onco-metabolite, 2-hydroxyglutarate (2-HG), that interferes with iron-dependent hydroxylase enzymes, including the TET family of 5'-methylcytosine hydroxylases. TET enzymes are critical for the dynamic regulation of DNA methylation. IDH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), though the functional significance of this altered epigenetic state remains unclear. Here we show that IDH1 mutant gliomas exhibit hyper-methylation at CTCF binding sites, leading to reduced binding of this methylation-sensitive insulator protein. Loss of CTCF binding is associated with a loss of insulation between topological domains and aberrant gene activation. We specifically demonstrate that loss of CTCF at a domain boundary permits a constitutive enhancer to aberrantly interact with the receptor tyrosine kinase gene PDGFRA, a prominent glioma oncogene. Treatment of IDH mutant gliomaspheres with demethylating agent partially restores insulator function and reduces PDGFRA expression. Conversely, CRISPR-mediated disruption of the CTCF binding sequence in IDH wildtype gliomaspheres induces PDGFRA expression and increases proliferation. Our study suggests that IDH mutations promote gliomagenesis by disrupting chromosomal topology and allowing aberrant regulatory interactions that induce oncogene expression. CTCF occupancy characterization and histone H3K27 acetylation profiling in IDH1 mutant and wild-type glioma patient specimens and culture models. ChIP-seq raw data is to be made available through dbGaP (controlled access) due to patient privacy concerns.

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