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Genetic stability in FA cells before and after gene editing and cell reprogramming.

ABSTRACT: Fibroblasts from a Fanconi anemia (FA) patient (FA-52) before and after correction by gene editing and transduction with a lentiviral vector expressing telomerase (geFA-52T fibroblasts). IPCs were generated from fibroblasts corrected by gene editing using STEMCCA LV (geFA-52T IPSCs clone 16) and finally the reprogramming cassette was excised (excised geFA-52T IPSCs clone 16.1)

ORGANISM(S): Homo sapiens

PROVIDER: GSE56790 | GEO | 2014/05/01

SECONDARY ACCESSION(S): PRJNA244595

REPOSITORIES: GEO

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Genetic stability in FA cells before and after gene editing and cell reprogramming.

Project description:Fibroblasts from a Fanconi anemia (FA) patient (FA-52) before and after correction by gene editing and transduction with a lentiviral vector expressing telomerase (geFA-52T fibroblasts). IPCs were generated from fibroblasts corrected by gene editing using STEMCCA LV (geFA-52T IPSCs clone 16) and finally the reprogramming cassette was excised (excised geFA-52T IPSCs clone 16.1) Four groups: Fibroblasts from a FA patient (FA-52) before and after correction by gene editing and transduction with a lentiviral vector expressing telomerase (geFA-52T) and gene editied IPSCs before and after excision of the reprogramming cassette (geFA-52T IPSCs clone 16 and excised geFA-52T IPSCs clone 16.1)

2014-05-01 | E-GEOD-56790 | biostudies-arrayexpress

Global gene expression analysis for neuron stem cells (NSC) derived from iPSCs with Fanconi Anemia

Project description:Fanconi Anemia (FA) is a recessive disorder associated with genomic instability We generated iPSC from FA patient fibroblasts and further corrected the mutated FANCA gene with a homologous recombination-based approach. The NSCs were differentiated from control-iPSCs, FA-iPSCs, and corrected FA-NSCs, and their gene expressions were determined by microarray analysis.

2014-06-14 | E-GEOD-40865 | biostudies-arrayexpress

Global gene expression analysis for neuron stem cells (NSC) derived from iPSCs with Fanconi Anemia

2014-06-14 | GSE40865 | GEO

Pluripotent cell models of Fanconi anemia identify the early pathological defect in human hemoangiogenic progenitors

Project description:Fanconi anemia (FA) is a disorder of genomic instability characterized by progressive bone marrow failure (BMF), developmental abnormalities and an increased susceptibility to cancer. Although various consequences in hematopoietic stem/progenitor cells have been attributed to FA-BMF, the quest to identify the initial pathological event is still ongoing. To address this issue, we established induced pluripotent stem cells (iPSCs) from fibroblasts of six FA patients with FANCA mutations. An improved reprogramming method yielded iPSC-like colonies from all patients, and iPSC clones were propagated from two patients. Quantitative evaluation of the differentiation ability demonstrated that the differentiation propensity toward the hematopoietic and endothelial lineages is already defective in early hemoangiogenic progenitors. The expression levels of critical transcription factors were significantly downregulated in these progenitors. These data indicate that the hematopoietic consequences in FA patients originate from the early hematopoietic stage, and highlight the potential usefulness of iPSC technology for elucidating the pathogenesis of FA-BMF. The investigation of the RNA-seq analysis of iPSC-derived HAPCs.

2015-02-03 | E-GEOD-65507 | biostudies-arrayexpress

FA Sequencing

Project description:Sequencing FA

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Project description:Sequencing FA

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Pluripotent cell models of Fanconi anemia identify the early pathological defect in human hemoangiogenic progenitors

2015-02-03 | GSE65507 | GEO

Modeling Fanconi Anemia pathogenesis and therapeutics using integration-free patient iPSCs

Project description:To elucidate the transcriptional and epigenetic alterations underlying the neurogenic defects of FA-NSCs, we conducted gene expression microarray analysis and global DNA methylation profiling. The gene expression pattern of gene-corrected NSCs (C-FA-NSCs) resembled that of control-NSCs but clustered distantly from FA-NSCs (Fig. 6F and Table S1). Hierarchical clustering based on DNA methylation levels in the promoter region (+/-1.5kb from TSS) of genes whose expression levels were rescued in C-FA-NSCs, placed C-FA-NSCs closer to control-NSCs and away from FA-NSCs (Fig. 6G), although this pattern was not seen at the whole genome level (Fig. S4C). This suggests that FANCA gene correction leads to specific methylation changes in a subset of promoters. Examination of the methylomes of NSCs derived from Fanconi Anemia iPSCs before and after gene correction by targeted bisulfite sequencing with padlock probes

2014-05-15 | E-GEOD-57685 | biostudies-arrayexpress

Transcription profiling of human bone marrow cells from normal volunteers and from children and adults with Fanconi anemia

Project description:Fanconi anemia (FA) is a rare inherited disease complicated by aplastic anemia. There is evidence that hematopoietic stem cells have lost self replicative capacity and undergo apoptosis when exposed to inhibitory cytokines including interferon gamma and tumor necrosis factor-alpha. We used gene expression microarrays to identify transcriptomal differences between bone marrow cells from normal volunteers and from children and adults with Fanconi anemia Experiment Overall Design: Fanconi anemia patients were identified using mitomycin C and/or diepoxybutane chromosomal breakage analysis. Eleven normal volunteers and 21 FA patients were studied. All FA patients with cytogenetic evidence of clonal evolution were excluded. All FA patients with acute leukemia were excluded. RNA was prepared from freshly obtained low density mononuclear cell fractions.

2009-09-18 | E-GEOD-16334 | biostudies-arrayexpress

Transcription profiling of hepatocyes from Zucker fa/fa obese rats vs controls

Project description:Analysis of the gene signature of steatosis associated to obesity in hepatocytes of Zucker fa/fa obese rats and their controls; identifying target genes linked to steatosis progression. or Obesity and insulin resistance-associated steatosis can be a non-inflammatory condition affecting hepatocytes or progress to steatohepatitis: a condition that can result in end-stage liver disease. Although molecular events leading to accumulation of lipid droplets in the liver have been identified individually, the complexity of the condition suggested that emergent target would be uncovered by a more comprehensive examination. Then, this study was aimed at establishing a gene signature of steatosis in hepatocytes and at identifying target genes linked to steatosis progression. Using Affymetrix oligonucleotide arrays, we compared transcriptomes of hepatocytes isolated from Zucker "fa/fa" obese rats with three different age-related grades of steatosis with those of their counterpart non-steatotic cells.

2008-07-31 | E-MEXP-1414 | biostudies-arrayexpress

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