Ontology highlight
ABSTRACT:
PROVIDER: PRJNA597052 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10749074.fastq.gz | Fastqsanger.gz | |||
| SRR10749075.fastq.gz | Fastqsanger.gz | |||
| SRR10749076.fastq.gz | Fastqsanger.gz | |||
| SRR10749077_1.fastq.gz | Fastqsanger.gz | |||
| SRR10749077_2.fastq.gz | Fastqsanger.gz |
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Project description:Ependymomas exist within distinct genetic subgroups, but the molecular diversity within individual ependymomas is unknown. We performed multiplatform molecular profiling of 6 spatially-distinct samples from an ependymoma with C11orf95-RELA fusion. DNA methylation and RNA sequencing distinguished clusters of samples according to neuronal development gene expression programs that could also be delineated by differences in magnetic resonance blood perfusion. Exome sequencing and phylogenetic analysis revealed epigenomic intratumor heterogeneity, and suggested that chromosomal structural alterations may precede accumulation of single nucleotide variants during ependymoma tumorigenesis. In sum, these findings shed new light on the oncogenesis and intratumor heterogeneity of ependymoma.
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Project description:Cancer is a disease of the genome. Many genomic abnormalities have been found in a variety of cancer types, which are believed to be attributable to tumorigenesis as well as resistance to treatment and recurrence. Genomic heterogeneity in the same type of cancer or within a tumor reveals the complexity of cancer biology so that intratumor heterogeneity has become an inherent feature of cancer. In this study, we use whole-exome sequencing and array comparative genomic hybridization technology to examine the mutational profiling and copy number changes from multi-region samples within an esophageal cancer in order to understand the genomic phylogeny in the evolution of intratumor heterogeneity in esophageal cancer.
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Project description:Multiple stereotatically separate sites from human meningioma were processed for methlyation profiling Meningiomas are the most common primary intracranial tumors, but the molecular drivers of meningioma tumorigenesis are poorly understood. We hypothesized that investigating intratumor heterogeneity in meningiomas would elucidate biologic drivers and reveal new targets for molecular therapy. To test this hypothesis, we performed multiplatform molecular profiling of 86 spatially-distinct samples from 13 human meningiomas. Our data reveal that regional alterations in chromosome structure underlie clonal transcriptomic, epigenomic, and histopathologic signatures in meningioma. Stereotactic co-registration of sample coordinates to preoperative magnetic resonance images further demonstrated that high apparent diffusion coefficient (ADC) distinguished meningioma regions with proliferating cells enriched for developmental gene expression programs. To understand the function of these genes in meningioma, we developed a human cerebral organoid model of meningioma and validated the high ADC marker genes CDH2 and PTPRZ1 as potential targets for meningioma therapy using live imaging, single cell RNA sequencing, CRISPR interference, and pharmacology.
2020-06-17 | GSE151067 | GEO
Project description:Intratumor mutational heterogeneity has been documented in primary non-small cell lung cancer. Here, we elucidate mechanisms of tumor evolution and heterogeneity in metastatic thoracic tumors (lung adenocarcinoma and thymic carcinoma) using whole-exome and transcriptome sequencing, SNP array for copy number alterations (CNA) and mass spectrometry-based quantitative proteomics of metastases obtained by rapid autopsy. APOBEC-mutagenesis, promoted by increased expression of APOBEC3 region transcripts and associated with a high-risk germline APOBEC3 variant, strongly correlated with mutational tumor heterogeneity. TP53 mutation status was associated with APOBEC hypermutator status. Interferon pathways were enriched in tumors with high APOBEC mutagenesis and IFN- induced expression of APOBEC3B in lung adenocarcinoma cells in culture suggesting a role for the immune microenvironment in the generation of mutational heterogeneity. CNA occurring late in tumor evolution correlated with downstream transcriptomic and proteomic heterogeneity, although global proteomic heterogeneity was significantly greater than transcriptomic and CNA heterogeneity. These results illustrate key mechanisms underlying multi-dimensional heterogeneity in metastatic thoracic tumors.
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Project description:Gene expression (mRNA) profiling of human ependymomas Despite the histological similarity of ependymomas from throughout the neuraxis, the disease likely comprises multiple independent entities, each with a distinct molecular pathogenesis. Transcriptional profiling of two large independent cohorts of ependymoma reveals the existence of two demographically, transcriptionally, genetically, and clinically distinct groups of posterior fossa (PF) ependymoma. Group-A patients are younger, have laterally located tumors with a balanced genome, and are much more likely to exhibit recurrence, secondary metastasis, and death as compared to Group-B patients. Identification and optimization of immunohistochemical markers for PF ependymoma subgroups allowed validation of our findings on a third independent group of tumors using a human ependymoma tissue microarray, and provides a tool for prospective prognostication and stratification of PF ependymoma patients. We analyzed 102 primary ependymomas on the Affymetrix Exon 1.0ST platform (Gene Level).
2011-08-14 | E-GEOD-27279 | biostudies-arrayexpress
Project description:Despite histological similarity of ependymomas from throughout the neuraxis, the disease likely comprises multiple independent entities, each with a distinct molecular pathogenesis. Transcriptional profiling of two large independent cohorts of ependymomas reveals the existence of two demographically, transcriptionally, genetically and clinically distinct groups of posterior fossa (PF) ependymoma. Group A patients are younger, have laterally located tumors with a balanced genome, and are much more likely to exhibit recurrence, metastasis, and death as compared to Group B patients. Identification and optimization of immunohistochemical markers for PF ependymoma subgroups allowed validation of our findings on a third group of independent ependymomas using a human ependymoma tissue microarray, and provides a tool for prospective prognostication and stratification of PF ependymoma patients. This SuperSeries is composed of the following subset Series: GSE27283: Human ependymoma samples [expression] GSE27286: Human ependymoma samples, Subgrouping [aCGH - German Cancer Research Center human 33K BAC array] Refer to individual Series
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Project description:We classified samples and deciphered a key genes signature of intratumor heterogeneity by Principal Component Analysis and Weighted Gene Co-expression Network Analysis. At the genome level, we identified common GB copy number alterations and but a strong inter-individual molecular heterogeneity.
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Project description:Lung adenocarcinoma (ADC) is the most prevalent subtype of lung cancer and characterized by considerable morphological and mutational heterogeneity. However, little is known about the epigenomic intratumor variability between spatially separated histological growth patterns of ADC. In order to reconstruct the clonal evolution of histomorphological growth patterns, we performed global DNA methylation profiling of 27 primary tumor regions, seven matched normal tissues, and six lymph node metastases from seven ADC cases. Additionally, we investigated the methylation data from 369 samples of the TCGA ADC cohort. All regions showed varying degrees of methylation changes between segments of different, but also of the same growth patterns. Similarly, copy number variations were seen between spatially distinct segments of each patient. Hierarchical clustering of promoter methylation revealed extensive heterogeneity within and between the cases. Intra-tumor DNA methylation heterogeneity demonstrated a branched clonal evolution of ADC regions driven by genomic instability with subclonal copy number changes. Notably, methylation profiles within tumors were not more similar to each other than to those from other individuals. In two cases, different tumor regions of the same individuals were represented in distant clusters of the TCGA cohort, illustrating the extensive epigenomic intratumor heterogeneity of ADCs. Importantly, we found no evidence for the lymph node metastases to be derived from a common growth pattern. Instead, they had evolved early and separately from a particular pattern in each individual primary tumor. In summary, our results suggest that extensive variation of epigenomic features contributes to the molecular and phenotypic heterogeneity of primary ADCs and lymph node metastases.
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