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Investigation of the mechansim underlying the inflammatory phenotype in Group A ependymoma

ABSTRACT: Inflammatory response has been identified as a molecular signature of high-risk Group A ependymoma (EPN). To better understand the biology of this phenotype and aid therapeutic development, transcriptomic data from Group A and B EPN patient tumor samples, and additional malignant and normal brain data, were analyzed to identify the mechanism underlying EPN group A inflammation. Gene expression profiles of Group A and B EPN were contrasted to identify inflammatory transcriptional profiles (GSEA analysis). Candidate inflammatory mechanism genes were examined across a broader cohort of pediatric and adult brain tumor types and normal brain.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66354 | GEO | 2015/02/27

SECONDARY ACCESSION(S): PRJNA276629

REPOSITORIES: GEO

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Investigation of the mechansim underlying the inflammatory phenotype in Group A ependymoma

Project description:Inflammatory response has been identified as a molecular signature of high-risk Group A ependymoma (EPN). To better understand the biology of this phenotype and aid therapeutic development, transcriptomic data from Group A and B EPN patient tumor samples, and additional malignant and normal brain data, were analyzed to identify the mechanism underlying EPN group A inflammation. Gene expression profiles of Group A and B EPN were contrasted to identify inflammatory transcriptional profiles (GSEA analysis). Candidate inflammatory mechanism genes were examined across a broader cohort of pediatric and adult brain tumor types and normal brain. Gene expression profiles were generated from surgical tumor and normal brain samples (n=149) using Affymetrix HG-U133plus2 chips (Platform GPL570).

2015-02-27 | E-GEOD-66354 | biostudies-arrayexpress

RNA sequencing of posterior fossa ependymoma harboring 6q loss

Project description:Two distinct groups of posterior fossa ependymoma, PF-EPN-A and PF-EPN-B have been identified in children and are often associated with widely distinct outcomes. We have identified an ultra-high-risk PF-EPN-A ependymoma with 6q loss. We performed RNA sequencing of posterior fossa ependymoma A (PF-EPN-A) tumor samples with chromosome 6q loss and balanced to understand the differences in 6q loss at the transcriptomic level

2021-02-15 | GSE164292 | GEO

Ependymoma subpopulation lineages underlie clinical classification and outcome (scRNAseq data set)

Project description:Ependymoma (EPN) is a brain tumor commonly presenting in childhood that remains fatal in the majority of children. Intra-tumoral cellular heterogeneity in bulk tumor samples significantly confounds our understanding of EPN biology, impeding development of effective therapy. We used single-cell RNA sequencing to identify four neoplastic cell subpopulations in posterior fossa EPN patient samples that underlie traditional subgroup classification and harbor divergent lineage trajectories and clinical outcomes. Neoplastic subpopulations expressed gene signatures associated with normal ependyma, ependymoma, and mesenchymal phenotypes, consequently named ciliated (CEC), transportive (TEC), undifferentiated (UEC), and mesenchymal ependymoma cells (MEC). The abundance of EPN subpopulations as estimated by deconvolution of EPN bulk tumor transcriptomes showed that the ratio of MEC and CEC cell fractions dictated assignment to the two main classification subgroups in PFA. Longitudinal analysis revealed evolution of subpopulation fractions, notably MEC and CEC, which changed between presentation and recurrence. Outcome analyses demonstrated that a higher proportion of UEC or MEC subpopulations was associated with shorter survival, whereas CEC was associated with longer survival. Unsupervised pseudotime analysis revealed divergent subpopulation lineages. The first lineage conformed to a classic cancer stem cell trajectory where UEC progenitors differentiate sequentially to TECs and then CECs. In the second trajectory MECs arise from UECs via TECs, potentially in response to hypoxia-mediated cellular stress, a process that we recreated in vitro in a hypoxia treated EPN cell line. Our study reveals the existence of significant, unappreciated cellular heterogeneity in EPN and provides important resolution of EPN tumor biology.

2020-07-31 | GSE125969 | GEO

Adult intracranial ependymoma - relevance of DNA methylation profiling for diagnosis, prognosis and treatment

Project description:Background: A methylation-based classification of ependymoma has recently found broad application. However, the diagnostic advantage and implications for treatment decisions remain unclear. Here, we retrospectively evaluate the impact of surgery and radiotherapy on outcome after molecular reclassification of adult intracranial ependymomas. Methods: Tumors diagnosed as intracranial ependymomas from 170 adult patients collected from eight diagnostic institutions were subjected to DNA methylation profiling. Molecular classes, patient characteristics, and treatment were retrospectively correlated with progression-free survival (PFS). Results: The classifier indicated an ependymal tumor in 73.5%, a different tumor entity in 10.6% and non-classifiable tumors in 15.9% of cases, respectively. The most prevalent molecular classes were posterior fossa ependymoma group B (EPN-PFB, 32.9%), posterior fossa subependymoma (PF-SE, 25.9%), and supratentorial ZFTA fusion-positive ependymoma (EPN-ZFTA, 11.2%). With a median follow-up of 60.0 months, the 5- and 10-year-PFS rates were 64.5% and 41.8% for EPN-PFB, 67.4% and 45.2% for PF-SE and 60.3% and 60.3% for EPN-ZFTA. In EPN-PFB, but not in other molecular classes, gross total resection (p=0.009) and postoperative radiotherapy (p=0.007) were significantly associated with improved PFS in multivariable analysis. Histological tumor grading (WHO 2 vs. 3) was not a predictor of prognosis within molecularly defined ependymoma classes. Conclusions: DNA methylation profiling improves diagnostic accuracy and risk stratification in adult intracranial ependymoma. The molecular class of PF-SE is unexpectedly prevalent among adult tumors with ependymoma histology and relapsed as frequently as EPN-PFB, despite the supposed benign nature. Gross total resection and radiotherapy may represent key factors in determining the outcome of EPN-PFB patients.

2023-02-21 | GSE224218 | GEO

Gene expression data from Brazilian pediatric ependymoma samples.

Project description:Ependymoma (EPN) is the third most common central nervous system (CNS) tumor in childhood and, recently, has been classified in nine robust molecular subgroups (Pajtler et al., 2015). However, molecular and clinical features of pediatric EPNs from Brazilian cohorts remain unexplored. Herein, we aimed to analyze the gene expression profile among three different molecular subgroups: ST-EPN-RELA, ST-EPN-YAP1 and PF-EPN-A.

2023-03-03 | GSE181162 | GEO

Ependymoma subpopulation lineages underlie clinical classification and outcome (microarray data set)

Project description:Introduction: single-cell RNA sequencing identified multiple subpopulations in childhood posterior fossa ependymoma. The contribution of individual neoplastic subpopulations to bulk tumor transcriptome-based molecular classification and patient outcome was estimated by deconvolution in a cohort of clinically-annotated primary and recurrent EPN samples. The abundance of EPN subpopulations was estimated in primary EPN samples and showed that the ratio of subpopulation fractions dictated assignment to the two main transcriptomic classification subgroups in childhood posterior fossa ependymoma. Longitudinal analysis revealed that subpopulation fractions changed between presentation and recurrence. Outcome analyses demonstrated that a different proportions of subpopulations were associated with differential survival.

2020-07-31 | GSE125861 | GEO

Characterization of Two Novel Ependymoma Cell Lines with Chromosome 1q gain derived from Posterior Fossa Tumors of Childhood

Project description:Introduction: Ependymoma (EPN) studies have revealed certain genetic markers, such as gain of chromosome 1q (1q+), as indicators of poor survival and high rate of recurrence. Development of novel therapeutics for EPN has been hampered by a lack of in vivo and in vivo models. We describe two unique 1q+ cell lines (811 and 928) derived from two children with metastatic, recurrent EPN. Both cell lines were characterized using histological, karyotypic and transcriptomic methods Transcriptomic analysis revealed that both lines, when cultured in 3D format, clustered closer to primary EPN tumors than monolayer format and with better fidelity of EPN-specific transcripts, namely those related to cilia function. Additionally, 3D culture histology revealed striking ependymal rosette formation, similar to primary tumors. Transcriptional enrichment of extracellular matrix, however, was a common signature of EPN primary tumor and cell lines in both monolayer and 3D formats.

2016-09-09 | GSE86574 | GEO

Epigenetic Landscape of Pediatric Ependymoma Recurrence

Project description:Pediatric ependymoma has relatively low frequencies of DNA mutations, which suggest that epigenetics may drive tumors. However, the epigenetic mechanisms for recurrent ependymoma are still poorly understood. Here, we performed longitudinal and comprehensive DNA methylation and gene expression analysis for recurrent pediatric ependymoma tumors from 10 patients, total 46 DNA methylomes (including primary tumors and matched recurrent tumors; normal pediatric brain tissues and PDOX tumors). Both RELA and PFA tumors maintained the subtype DNA methylation signatures during repeated relapses. We further identified the potential DNA methylation predictors, drivers and boosters and their potential regulated genes for recurrent ependymoma tumors. Increased DNA methylation levels within H3K4me1 enriched regions indicates disturbed functions of LSD1 gene in recurrent ependymoma tumors. Combining novel LSD1 inhibitor SYC-836 with radiation (XRT) significantly prolonged animal survival times in PDOX models of recurrent PFA ependymoma. Our PDOX models provide a unique platform for preclinical testing drugs and development of new therapy for pediatric recurrent ependymoma.

2022-07-12 | GSE156619 | GEO

Expression data from paediatric ependymoma short-term cell cultures

Project description:Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours. To identify targets of epigenetic silencing mediated by CpG island methylation in paediatric ependymoma, we used a pharmacological unmasking approach through treatment with the demethylating agent 5-Aza-2M-bM-^@M-^Y-deoxycytidine followed by global expression microarray analysis. Three short-term ependymoma cell cultures were used for whole genome expression analysis following treatment with the demethylating agent 5-Aza-dC (5 M-BM-5mol/L) or mock-treated with DMSO (M-bM-^IM-$0.1% v/v) for 96-hrs.

2013-12-02 | E-GEOD-45437 | biostudies-arrayexpress

PFA ependymoma primary and recurring tumors show differences in cellularity, DNA methylation and relevant copy number variations.

Project description:Posterior fossa type A (PF-EPN-A, PFA) ependymoma are aggressive tumors that mainly affect children and have a poor prognosis. Histopathology shows significant intratumoral heterogeneity, ranging from loose tissue to often sharply demarcated, extremely cell dense tumor areas. To determine molecular differences in morphologically different areas and to understand their clinical significance, we analyzed 113 PF-EPN-A samples, including 40 corresponding relapse samples. Relapsing tumors displayed a higher proportion of cell dense areas (p=0.036), a change in PF-EPN-A methylation subtypes (13/32 patients), and novel chromosome 1q gains and 6q losses (12/32 cases) compared to corresponding primary tumors.

2024-01-31 | GSE248617 | GEO

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