11768 results for "cancer rna-seq"

in 13.44 milliseconds.

• Evolving Cell States and Oncogenic Drivers during the Progression of IDH-Mutant Gliomas

  The study aims to understand the changes in cell states during the progression of IDH mutant gliomas. We generated scATAC-seq data from tumor samples of patients with IDH mutant gliomas, ranging from grade 2 to grade 4, including both IDH mutant oligodendroglioma and IDH mutant astrocytoma samples. Additionally, we have generated scRNA-seq data from patient-derived organoids that were treated with a DNMT1 inhibitor.

  Study phs003697

• Gene regulation of human stimulated and cultured CD4+ Treg cells

  This dataset maps gene expression regulation in human primary regulatory CD4+ T cells (Tregs) stimulated using PMA and ionomycin or cultured without stimulus for 18 hours. It includes whole genome sequence data for ChM-seq (18 H3K4me3, 20 H3K27ac and 3 inputs), ATAC-seq (42 samples) and whole transcriptome (39 samples). All individuals were genotyped using coreExome Illumina SNP chip array (included in EGAS00001003516).

  Study EGAS00001003515

• Next generation sequencing of diffuse intrinsic pontine glioma samples to identify recurrent mutations, variations, and expression patterns to define novel therapies

  Diffuse intrinsic pontine glioma (DIPG) is an extremely rare (~350 cases/year) and universally fatal childhood brain cancer. Standard clinical strategies such as chemotherapy and radiotherapy show only transient improvement in patient condition and result in negligible change in survival, DIPG remains at below 1% survival after 5 years. Prioritization of panobinostat through previous cooperative work resulted in a phase 1 clinical trial. Nonetheless, new therapies for DIPG must be identified to further dramatically change the statistics for DIPG. To identify novel therapy strategies for DIPG, we performed whole exome(16 new samples, 22 previously published samples, 38 in total with 26 matched normal) and RNA deep sequencing (17 new samples, 11 previously published samples) on a cohort of new patient samples. Sequencing results aid in the identification of recurrent mutations/variations and endotypic expression profiling to identify new therapeutic and treatment strategies for DIPG.

  Study phs001526

• MP2PRT-MNG: Identifying Novel Molecular Markers of Response to Radiotherapy in Meningiomas Using Samples from the RTOG-0539 (NCT00895622)

  The Molecular Profiling to Predict Response to Treatment (MP2PRT) program is part of the NCI's Cancer Moonshot Initiative. The aim of this program is the retrospective characterization and analysis of biospecimens collected from completed NCI-sponsored trials of the National Clinical Trials Network and the NCI Community Oncology Research Program. NRG RTOG (Radiation Therapy Oncology Group)-0539, which was a nonrandomized phase II cooperative group trial in 2009, was selected for inclusion in this program. NRG RTOG-0539 assigned patients with histologically confirmed diagnosis of meningioma to 1 of 3 risk groups based on 2007 WHO grade, resection extent, and recurrence status, and radiotherapy was given per protocol to the intermediate- and high-risk cases. Under the MP2PRT program, DNA methylation profiling, RNA sequencing, and whole exome sequencing were performed on clinical trial cases with available tissue for molecular analyte extraction and subsequent sequencing. Raw molecular data with metadata are available for this study.

  Study phs003707

• Nivolumab plus chemotherapy or ipilimumab in gastroesophageal cancer: CheckMate 649 biomarker analyses

  First-line nivolumab-plus-chemotherapy demonstrated superior overall survival (OS) versus chemotherapy for advanced gastroesophageal adenocarcinoma (CheckMate 649). Nivolumab-plus-ipilimumab provided durable responses and higher survival rates versus chemotherapy; however, the prespecified OS significance boundary was not met. To identify biomarkers predictive of differential efficacy outcomes, exploratory analyses were performed using whole-exome sequencing and RNA sequencing. Nivolumab-based therapies demonstrated improved efficacy versus chemotherapy in hypermutated and, to a lesser degree, Epstein Bar Virus-positive tumors compared with chromosomally unstable and genomically stable tumors. Within the KRAS-altered subgroup, only patients treated with nivolumab-plus-chemotherapy demonstrated improved OS benefit versus chemotherapy. Low stroma gene expression signature scores were associated with OS benefit with nivolumab-based regimens; high regulatory T-cell signatures were associated with OS benefit only with nivolumab-plus-ipilimumab. Our analyses suggest that distinct and overlapping pathways contribute to the efficacy of nivolumab-based regimens in gastroesophageal adenocarcinoma.

  Study EGAS50000000747

• Epigenomics and Single-cell Sequencing Define a Developmental Hierarchy in Langerhans Cell Histiocytosis

  Langerhans cell histiocytosis (LCH) is a rare neoplasm predominantly affecting children. It occupies a hybrid position between cancers and inflammatory diseases, and it provides an attractive model for studying cancer development. To explore the molecular mechanisms underlying the pathophysiology of LCH and its characteristic clinical heterogeneity, we investigated the transcriptomic and epigenomic diversity in primary LCH lesions. Using single-cell RNA sequencing, we identified multiple recurrent types of LCH cells within these biopsies, including putative LCH progenitor cells and several subsets of differentiated LCH cells. We confirmed the presence of proliferative LCH cells in all analysed biopsies using immunohistochemistry, and we defined an epigenomic and gene-regulatory basis of the different LCH cell subsets by chromatin accessibility profiling. In summary, our single-cell analysis of LCH uncovered an unexpected degree of cellular, transcriptomic, and epigenomic heterogeneity among LCH cells, indicative of complex developmental hierarchies in LCH lesions.

  Study EGAS00001003822

• Comprehensive Genomic and Transcriptomic Analysis of Rare Cancers for Guiding of Therapy (H021)

  Here we analyzed the molecular profiles and clinical outcomes of 1,310 patients (proportion of rare cancers, 75%) enrolled in a prospective observational study by the German Cancer Consortium that applies whole-genome/exome and RNA sequencing to inform the care of adults with incurable cancers. Based on 472 single and six composite biomarkers, a cross-institutional molecular tumor board provided evidence-based management recommendations, including diagnostic reevaluation, genetic counseling, and experimental treatment, in 88% of cases. Recommended therapies were administered in 362 of 1,138 patients (31.8%) and resulted in significantly improved response and disease control rates (23.9% and 55.3%, respectively) compared to previous therapies, translating into a progression-free survival ratio >1.3 in 35.7% of patients.

  Study EGAS00001004813

• The Proteogenomic Subtypes of Acute Myeloid Leukemia

  Acute myeloid leukemia (AML) is an aggressive blood cancer with poor prognosis. We report a comprehensive proteogenomic analysis of bone-marrow biopsies from 252 uniformly treated AML patients to elucidate the molecular pathophysiology of AML in order to inform future diagnostic and therapeutic approaches. In addition to in-depth quantitative proteomics, our analysis includes cytogenetic profiling and DNA/RNA sequencing. We identify five proteomic AML subtypes, each reflecting specific biological features spanning genomic boundaries. Two of these proteomic subtypes correlate with patient outcome, but none are exclusively associated with specific genomic aberrations. Remarkably, one subtype (Mito-AML), which is only captured in the proteome, is characterized by high expression of mitochondrial proteins and confers poor outcome, with reduced remission rate and shorter overall survival upon treatment with intensive induction chemotherapy. Functional analyses reveal that Mito-AML is metabolically wired towards stronger complex I dependent respiration and is more responsive to treatment with the BCL2 inhibitor venetoclax.

  Study EGAS00001005950

• TGF-β attenuates tumour response to PD-L1 blockade by contributing to exclusion of T cells.

  We examined tumours from a large cohort of patients with metastatic urothelial bladder cancer (mUC) treated with an anti–PD-L1 agent (atezolizumab) and identified major determinants of clinical response and immune escape. Whole transcriptome profiles were generated for 368 patients using TruSeq RNA Access technology (Illumina). Somatic mutations were determined via whole exome sequencing for a subset of these patients. - Response was associated with CD8+ T effector cell phenotype and, to an even greater extent, high neoantigen or tumour mutation burden (TMB). On the other hand, lack of response was associated with a transforming growth factor β (TGF-β) signature, particularly in patients with CD8+ T cells preferentially residing in collagen-rich matrix surrounding tumours. Integration of these three independent biological features provided the best basis for understanding outcome in this setting. -

  Study EGAS00001002556

• ICGC MMML-seq Data Freeze November 2012 whole genome sequencing

  ICGC MMML-seq Data Freeze November 2012 whole genome sequencing

  Dataset EGAD00001000278

• ICGC MMML-seq Data Freeze November 2012 whole exome sequencing

  ICGC MMML-seq Data Freeze November 2012 whole exome sequencing

  Dataset EGAD00001000279

• ICGC MMML-seq Data Freeze March 2013 whole genome sequencing

  ICGC MMML-seq Data Freeze March 2013 whole genome sequencing

  Dataset EGAD00001000355

• ICGC MMML-seq Data Freeze July 2013 transcriptome sequencing

  ICGC MMML-seq Data Freeze July 2013 transcriptome sequencing

  Dataset EGAD00001000648

• EM-seq converted WGS for CSF-derived cfDNA from pediatric brain tumor patients

  EM-seq converted WGS for CSF-derived cfDNA from pediatric brain tumor patients

  Dataset EGAD50000001975

• Patient data used in FLTseq paper

  Apply newly developed FLT-seq protocol and package FLAMES on a primary patient sample

  Study EGAS00001005597

• Reference epigenome Pancreas-Islet07 h3k9me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet07 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007462

• Reference epigenome ADMSC02_smRNA-Seq data generated from KEP study

  A ADMSC02_smRNA-Seq single end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003868

• Reference epigenome IPS-NPC01 input ChIP-Seq data generated from KEP study

  IPS-NPC01 input ChIP-Seq paired end data

  Dataset EGAD00001007283

• Reference epigenome Pancreas-Islet02 input ChIP-Seq data generated from KEP study

  Pancreas-Islet02 input ChIP-Seq paired end data

  Dataset EGAD00001007199

• Reference epigenome Pancreas-Islet02 h3k9me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007198

• Reference epigenome Pancreas-Islet04 h3k4me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007211

• Reference epigenome IPS-ENeuron02 h3k4me3 ChIP-Seq data generated from KEP study

  IPS-ENeuron02 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007302

• Reference epigenome Pancreas-Islet07 h3k4me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet07 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007461

• Reference epigenome Fat-adipocyte04 h3k9me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007483

• Reference epigenome ADMSC03_smRNA-Seq data generated from KEP study

  A ADMSC03_smRNA-Seq single end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003869