Expression data from +7 hNPCs and diploid hNPCs
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18349 | GEO | 2009/10/01
SECONDARY ACCESSION(S): PRJNA118095
REPOSITORIES: GEO
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Project description:Human Neural progenitor cells have been found to have karyotypic abnormalities. In this study we explored the gene changes between hNPCs that are karyotypically normal and hNPCs with a trisomy of chromosome 7. We used Affymetrix GeneChips to study gene expression changes between karyotypically normal hNPCs and trisomy 7 hNPCs. Cells grown in culture for ~20 passages from diploid and + 7 hNPCs were selected for RNA extraction and hybridization on Affymetrix microarrays.
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Project description:The aim of this study was to analyze global changes of gene expression in lymphocytes from children with trisomy 21 by means of the serial analysis of gene expression (SAGE) methodology. Comparison between DS and normal profiles revealed that most of the transcripts were expressed at similar levels. Among the 242 significantly differentially expressed SAGE tags, many of them corresponded to genes involved in transcription, RNA processing, signaling, immune response and lipid metabolism. Our results indicate that trisomy 21 induces a modest dysregulation of disomic genes that may be related to the immunological perturbations seen in DS. Keywords: SAGE analysis in normal and Down syndrome lymphocytes Lymphocytes were isolated from peripheral blood of normal and karyotypically confirmed full trisomy 21 children. Children included in the study, ranging in age from 1-4 years, were self reported as free of chronic or acute infections. Total RNA was isolated with TRIzol reagent (Invitrogen). The SAGE libraries were constructed using pooled RNA from six DS children (DS library) and six normal children (control group) to eliminate any individual variation. SAGE was performed by means of the I-SAGE kit (Invitrogen) following the manufacturer’s instructions.
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Project description:Acute promyelocytic leukemia (APL) is a hematopoietic malignant disease characterized by the chromosomal translocation t(15;17), resulting in the formation of the PML-RARA gene. Here, 47 t(15;17) APL samples were analyzed with high-density single-nucleotide polymorphism microarray (50K and 250K SNP-chips) using the new algorithm AsCNAR (allele-specific copy-number analysis using anonymous references). Copy-number-neutral loss of heterozygosity (CNN-LOH) was identified at chromosome 10q (3 cases), 11p (3 cases) and 19q (1 case). Twenty-eight samples (60%) did not have an obvious alteration (normal-copy-number [NC] group). Nineteen samples (40%) showed either one or more genomic abnormalities: 8 samples (17%) had trisomy 8 either with or without an additional duplication, deletion, or CNN-LOH (+8 group); and 11 samples (23%) had genomic abnormalities without trisomy 8 (other abnormalities group). These chromosomal abnormalities were acquired somatic mutations. Interestingly, FLT3-ITD mutations (11/47 cases) only occurred in the group with no genomic alteration (NC group). Taken together, these results suggest that the pathway of development of APL differs in each group: FLT3-ITD, trisomy 8, and other genomic changes. Here, we showed for the first time hidden abnormalities and novel disease-related genomic changes in t(15;17) APL. Keywords: SNP-chip
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