Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA237315 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Detection of aberrant DNA methylation in undifferentiated and differentiated human ES cells compared to normal fetal tissues
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Project description:we establish a 272 Chinese STS patients cohort containing 12 sarcoma subtypes, well-differentiated liposarcoma (WDLPS), myxoid liposarcoma (MLPS), dedifferentiated liposarcoma (DDLPS), angiosarcoma (AS), undifferentiated sarcoma (UPS), myxofibrosarcoma (MFS), other fibroblastic/myofibroblastic tumors (otherFS), leiomyosarcoma (LMS), rhabdomyosarcoma (RMS), malignant peripheral nerve sheath tumor (MPNST), synovial sarcoma (SS), and epithelioid sarcoma (ES).
2024-01-03 | PXD047297 | iProX
Project description:Promoter methylation was assayed in a number of breast cancer and control normal samples along with the effects of 5'-aza-2'-deoxycytidine on breast cancer cell line transcriptomes. Aberrant promoter hypermethylation is frequently observed in cancer. The potential for this to contribute to tumour development depends on whether the genes affected are repressed because of their methylation. Many aberrantly methylated genes play important roles in development and are bivalently marked in ES cells suggesting that their aberrant methylation may reflect developmental processes. We investigated this possibility by analysing promoter methylation in 19 breast cancer cell lines, 10 normal tissues and 47 primary breast tumours. In order to determine the role of DNA methylation in silencing genes in breast cancer, we also examined the effects of the demethylating agent 5-aza-2?-deoxycytidine on gene expression in 3 breast cancer cell lines and HCT116 cells. Gene expression changes were also assayed in the DNA methyltransferase deficient HCT116 DKO cell line. Our findings implicate aberrant DNA methylation as a marker of cell lineage rather than tumour progression and suggest that, in most cases, it does not cause the repression with which it is associated. A number of human breast cancer cell lines, breast tumours and normal tissues were analysed on Illumina Infinium Methylation27 Beadchips to assay promoter methylation. Selected cell lines were analysed on expression arrays before and after treatment with 5-aza-2'-deoxycytidine.
2011-03-07 | E-GEOD-26990 | biostudies-arrayexpress
Project description:Promoter methylation was assayed in a number of breast cancer and control normal samples along with the effects of 5'-aza-2'-deoxycytidine on breast cancer cell line transcriptomes. Aberrant promoter hypermethylation is frequently observed in cancer. The potential for this to contribute to tumour development depends on whether the genes affected are repressed because of their methylation. Many aberrantly methylated genes play important roles in development and are bivalently marked in ES cells suggesting that their aberrant methylation may reflect developmental processes. We investigated this possibility by analysing promoter methylation in 19 breast cancer cell lines, 10 normal tissues and 47 primary breast tumours. In order to determine the role of DNA methylation in silencing genes in breast cancer, we also examined the effects of the demethylating agent 5-aza-2?-deoxycytidine on gene expression in 3 breast cancer cell lines and HCT116 cells. Gene expression changes were also assayed in the DNA methyltransferase deficient HCT116 DKO cell line. Our findings implicate aberrant DNA methylation as a marker of cell lineage rather than tumour progression and suggest that, in most cases, it does not cause the repression with which it is associated.
2011-03-07 | GSE26990 | GEO
Project description:Blood and endothelial cells arise from hemangiogenic progenitors that are specified from FLK1-expressing mesoderm by the transcription factor ETV2. FLK1 mesoderm also contributes to other tissues, including vascular smooth muscle (VSM) and cardiomyocytes. However, the developmental process of FLK1 mesoderm generation and its derivatives and the lineage relationship among FLK1 mesoderm derivatives these tissues remain obscure. Recent single cell RNA-sequencing (scRNA-seq) studies of early stages of embryogenesis embryos, or in vitro differentiated human embryonic stem (ES) cells have differentiation provided unprecedented information on the spatiotemporal resolution of cells in embryogenesis. Nonetheless, these snapshots still nonetheless offer insufficient information on dynamic developmental processes due to inadvertently missing intermediate states and unavoidable batch effects. Here we performed scRNA-seq of mouse ES cells in asynchronous embryoid bodies (EBs), in vitro differentiated embryonic stem (ES) cells containing undifferentiated ES cells and its differentiated hemangiogenic progeny, as well as yolk sacs, the first hematopoietic extraembryonic tissue in developing embryo that contains hemangiogenic and VSM lineages. We captured a continuous developmental process from undifferentiated pluripotent cells to FLK1 mesoderm-derived tissues involved in hemangiogenesis. This continuous transcriptome map will benefit both basic and applied studies of mesoderm and its derivatives.
2019-11-25 | GSE130146 | GEO
Project description:The directed differentiation of induced pluripotent stem (iPS) and embryonic stem (ES) cells into definitive endoderm (DE) would allow the derivation of otherwise inaccessible progenitors for endodermal tissues. However, a global comparison of the relative equivalency of DE derived from iPS and ES populations has not been performed. Recent reports of molecular differences between iPS and ES cells have raised uncertainty as to whether iPS cells could generate autologous endodermal lineages in vitro. Here, we have shown that both mouse iPS and parental ES cells exhibited highly similar in vitro capacity to undergo directed differentiation into DE progenitors. With few exceptions, both cell types displayed similar surges in gene expression of specific master transcriptional regulators and global transcriptomes that define the developmental milestones of DE differentiation. Microarray analysis showed considerable overlap between the genetic programs of DE derived from ES/iPS cells in vitro and authentic DE from mouse embryos in vivo. Intriguingly, iPS cells exhibited aberrant silencing of imprinted genes known to participate in endoderm differentiation, yet retained a robust ability to differentiate into DE. Our results show that, despite some molecular differences, iPS cells can be efficiently differentiated into DE precursors, reinforcing their potential for development of cell-based therapies for diseased endodermal-derived tissues. Comparison of mouse ES cells, mouse iPS cells, and E8.25 Mouse embryos; in the undifferentiated state and definitive endoderm differentiated state. ckit+/Sox2dim =definitive endoderm (day 5 of differentiation in vitro); Sox2bright =undifferentiated ES or iPS cells (day 0 of differentiation); ENDM1+/Epcam+/SSlo=foregut endoderm sorted from mouse E8.25 embryos; Epcam+/ENDM1 negative =sorted comparison population from mouse E8.25 embryos.
2011-03-31 | E-GEOD-27087 | biostudies-arrayexpress