PMCDS000ABU - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001015418 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Creation of living organoid biobank for ewing and ewing-like sarcomas
| EGAD00001015417 | EGA
Project description:Creation of living organoid biobank for ewing and ewing-like sarcomas
| EGAD00001015419 | EGA
Project description:Prospective derivation of a 'Living Organoid Biobank' of colorectal cancer patients
| PRJNA273501 | ENA
Project description:Prospective derivation of a 'Living Organoid Biobank' of colorectal cancer patients
| PRJNA270877 | ENA
Project description:In Rspondin-based 3D cultures, Lgr5 stem cells from multiple organs form ever-expanding epithelial organoids that retain their tissue identity. We report the establishment of tumor organoid cultures from 20 consecutive colorectal (CRC) patients. For most, organoids were also generated from adjacent normal tissue. The organoids closely resemble the original tumor. The spectrum of genetic changes observed within the 'living biobank' agrees well with previous large-scale mutational analyses of CRC. Gene expression analysis indicates that the major CRC molecular subtypes are represented. Tumor organoids are amenable to robotized, high-throughput drug screens allowing detection of gene-drug associations. As an example, a single organoid culture was exquisitely sensitive to Wnt secretion (porcupine) inhibitors and carried a mutation in the negative Wnt feedback regulator RNF43 (rather than in APC). Organoid technology may fill the gap between cancer genetics and patient trials, complement cell line- and xenograft-based drug studies and allow personalized therapy design. We generated organoids from healthy tissue and coloncarcinoma tissue. The organoids were trypsinized, plated in matrigel and overlaid with medium. After three days, RNA was isolated using Qiagen RNAeasy. Medium conditions are the same for all organoids, irrespective of their origin.
2015-05-07 | E-GEOD-64392 | biostudies-arrayexpress
Project description:The concept of Ewing family of tumors (EFT), characterized by FET-ETS fusions, has been recently challenged by the description of Ewing-like tumors with different gene fusions. Here we investigate the similarities and differences of FET-ETS, BCOR-CCNB3, CIC-DUX4 and EWSR1-NFATc2 tumors samples with a number of other sarcomas. Unsupervised clustering of gene expression profiles fully discriminates these four molecular entities. Specific gene signatures and pathways were further validated in model cell lines. While a clear inflammatory signature characterizes EWSR1-NFATc2 tumors, BCOR-CCNB3 and CIC-DUX4 exhibit high expression of homeobox and ETS protein families, respectively. We strongly suggest that abnormalities of chromatin remodeling may gather CIC-DUX4 and BCOR-CCNB3 tumors with rhabdoid tumors and synovial sarcomas. This dataset conains 14 CIC-DUX4 and 7 EWSR1-NFATc2 tumor samples as well as Human mesenchymal cell line expressing EWSR1-NFATc2 (duplicates) or mock treated (duplicates) and IB120 CIC-DUX4 cell line expressing an shRNA directed against CIC-DUX4 (4 replicates) or mock treated (duplicates).
2015-06-30 | E-GEOD-60740 | biostudies-arrayexpress
Project description:Transcriptome Profiling of Ewing Sarcomas
| PRJNA1124590 | ENA
Project description:We show that EWS-FLI1, an aberrant transcription factor responsible for the pathogenesis of Ewing sarcoma, reprograms gene regulatory circuits by directly inducing or directly repressing enhancers. At GGAA repeats, which lack regulatory potential in other cell types and are not evolutionarily conserved, EWS- FLI1 multimers potently induce chromatin opening, recruit p300 and WDR5, and create de novo enhancers. GGAA repeat enhancers can loop to physically interact with target promoters, as demonstrated by chromosome conformation capture assays. Conversely, EWS-FLI1 inactivates conserved enhancers containing canonical ETS motifs by displacing wild-type ETS transcription factors and abrogating p300 recruitment. ChIP-seq for of 4 histone modifications (H3K27ac, H3K4me1, H3K4me3 and H3K27me3), FLI1, p300, WDR5, ELF1 and GABPA in primary Ewing sarcomas, Ewing sarcoma cell lines (A673 and SKMNC cells), and mesenchymal stem cells (MSC). EWS-FLI1 was knocked down in Ewing sarcoma cell lines with lentiviral shRNAs (shFLI1 and shGFP control). EWS-FLI1 was expressed in MSCs with lentiviral expression vectors (pLIV EWSFLI1 or pLIV empty vector control). * Raw data not provided for the MSC and Primary Ewing sarcoma samples. *
2014-10-30 | E-GEOD-61944 | biostudies-arrayexpress
Project description:DNA methylation profiling has emerged as a valuable tool for tumor classification, exemplified by the German Cancer Research Center's creation of online classifiers for CNS tumors and sarcomas. Identification of rare molecular events, such as TRIO::TERT fusion in undifferentiated sarcomas, through DNA methylation profiling and transcriptome analysis aims to define distinct molecular subgroups within sarcomas of uncertain diagnosis, potentially improving classification and treatment strategies.In this study, we present 8 cases of sarcomas characterized by TRIO::TERT fusion, establishing it as a distinct molecular subtype of sarcomas. This fusion represents a consistent molecular feature across all analyzed tumors, suggesting its pivotal role in sarcomatogenesis. Identifying TRIO::TERT transcript sarcoma as a new tumor type may enhance diagnostic strategies for improved patient management.
2024-05-31 | GSE261891 | GEO
Project description:A "living biobank" of Crohn's Disease
| PRJNA793263 | ENA