Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA148481 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:G-banding of human embryonic stem cells (hESC) has proved their predisposition to aneuploidy of chromosomes 12, 17 and X. Now, using array-based comparative genomic hybridization, we find that hESC also accumulate other recurrent chromosomal abnormalities, such as duplications of stemness genes, submicroscopic instability of 20q11.21 and the appearance of a derivative chromosome 18. Keywords: comparative genomic hybridization, genomic integrity of human embryonic stem cells
2008-11-04 | GSE13422 | GEO
Project description:G-banding of human embryonic stem cells (hESC) has proved their predisposition to aneuploidy of chromosomes 12, 17 and X. Now, using array-based comparative genomic hybridization, we find that hESC also accumulate other recurrent chromosomal abnormalities, such as duplications of stemness genes, submicroscopic instability of 20q11.21 and the appearance of a derivative chromosome 18. Keywords: comparative genomic hybridization, genomic integrity of human embryonic stem cells Array-based comparative genomic hybridization was performed on 48 DNA samples from 17 human embryonic stem cell lines, all cultured in our laboratory under the same conditions. All lines were hybridized against DNA obtained from peripheral blood from donors with a known normal karyotype. No replicates were done from the same DNA sample, but, whenever possible the same stem cell line was analysed at later passages. All detected abnormalities were confirmed by FISH and/or G-banding.
2010-05-17 | E-GEOD-13422 | biostudies-arrayexpress
Project description:Pluripotent human embryonic stem cells were compared with essentially pure multipotent neural stem cell derivatives.
2016-07-13 | GSE39876 | GEO
Project description:Early childhood tumours arise from transformed embryonic cells, which often carry large copy number alterations (CNA). However, it remains unclear how CNAs contribute to embryonic tumourigenesis due to a lack of suitable models. Here we employ female human embryonic stem cell (hESC) differentiation and single-cell transcriptome and epigenome analysis to assess the effects of chromosome 17q/1q gains, which are prevalent in the embryonal tumour neuroblastoma (NB). We show that CNAs impair the specification of trunk neural crest (NC) cells and their sympathoadrenal derivatives, the putative cells-of-origin of NB. This effect is exacerbated upon overexpression of MYCN, whose amplification co-occurs with CNAs in NB. Moreover, CNAs potentiate the pro-tumourigenic effects of MYCN and mutant NC cells resemble NB cells in tumours. These changes correlate with a stepwise aberration of developmental transcription factor networks. Together, our results sketch a mechanistic framework for the CNA-driven initiation of embryonal tumours.
2024-03-22 | GSE221853 | GEO
Project description:Early childhood tumours arise from transformed embryonic cells, which often carry large copy number alterations (CNA). However, it remains unclear how CNAs contribute to embryonic tumourigenesis due to a lack of suitable models. Here we employ female human embryonic stem cell (hESC) differentiation and single-cell transcriptome and epigenome analysis to assess the effects of chromosome 17q/1q gains, which are prevalent in the embryonal tumour neuroblastoma (NB). We show that CNAs impair the specification of trunk neural crest (NC) cells and their sympathoadrenal derivatives, the putative cells-of-origin of NB. This effect is exacerbated upon overexpression of MYCN, whose amplification co-occurs with CNAs in NB. Moreover, CNAs potentiate the pro-tumourigenic effects of MYCN and mutant NC cells resemble NB cells in tumours. These changes correlate with a stepwise aberration of developmental transcription factor networks. Together, our results sketch a mechanistic framework for the CNA-driven initiation of embryonal tumours.
2024-03-22 | GSE219151 | GEO
Project description:Early childhood tumours arise from transformed embryonic cells, which often carry large copy number alterations (CNA). However, it remains unclear how CNAs contribute to embryonic tumourigenesis due to a lack of suitable models. Here we employ female human embryonic stem cell (hESC) differentiation and single-cell transcriptome and epigenome analysis to assess the effects of chromosome 17q/1q gains, which are prevalent in the embryonal tumour neuroblastoma (NB). We show that CNAs impair the specification of trunk neural crest (NC) cells and their sympathoadrenal derivatives, the putative cells-of-origin of NB. This effect is exacerbated upon overexpression of MYCN, whose amplification co-occurs with CNAs in NB. Moreover, CNAs potentiate the pro-tumourigenic effects of MYCN and mutant NC cells resemble NB cells in tumours. These changes correlate with a stepwise aberration of developmental transcription factor networks. Together, our results sketch a mechanistic framework for the CNA-driven initiation of embryonal tumours.
2024-03-22 | GSE219149 | GEO
Project description:Early childhood tumours arise from transformed embryonic cells, which often carry large copy number alterations (CNA). However, it remains unclear how CNAs contribute to embryonic tumourigenesis due to a lack of suitable models. Here we employ female human embryonic stem cell (hESC) differentiation and single-cell transcriptome and epigenome analysis to assess the effects of chromosome 17q/1q gains, which are prevalent in the embryonal tumour neuroblastoma (NB). We show that CNAs impair the specification of trunk neural crest (NC) cells and their sympathoadrenal derivatives, the putative cells-of-origin of NB. This effect is exacerbated upon overexpression of MYCN, whose amplification co-occurs with CNAs in NB. Moreover, CNAs potentiate the pro-tumourigenic effects of MYCN and mutant NC cells resemble NB cells in tumours. These changes correlate with a stepwise aberration of developmental transcription factor networks. Together, our results sketch a mechanistic framework for the CNA-driven initiation of embryonal tumours.
2024-03-22 | GSE262111 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE30652: Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and their Differentiated Derivatives [Illumina HT12v3 Gene Expression] GSE30653: Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and their Differentiated Derivatives [Illumina Infinium 27K DNA Methylation] GSE31848: Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and their Differentiated Derivatives [Illumina Infinium 450K DNA Methylation] Refer to individual Series
2012-05-13 | E-GEOD-30654 | biostudies-arrayexpress
Project description:By analyzing five human embryonic stem (hES) cell lines over long-term culture, we detected a recurrent genomic instability in the human genome. An amplification of 2.5â4.6 Mb at 20q11.21, encompassing about 23 genes in common, appeared in four cell lines of different origins. This amplification, which has been associated with oncogenic transformation, may provide a selective advantage to hES cells in culture Array-based comparative genomic hybridization, was performed on genomic DNA samples from different human embryonic stem cell lines, all cultured in our laboratory under the same conditions. VUB05-HD is an hES cell line carrying the Huntingtin mutant gene H1, H9, SA01, and VUB01 are various hES cell lines GSM341552 and GSM341553: SNP analysis GSM341589 to GSM341669: CGH analysis
2010-05-16 | E-GEOD-13565 | biostudies-arrayexpress
Project description:By analyzing five human embryonic stem (hES) cell lines over long-term culture, we detected a recurrent genomic instability in the human genome. An amplification of 2.5–4.6 Mb at 20q11.21, encompassing about 23 genes in common, appeared in four cell lines of different origins. This amplification, which has been associated with oncogenic transformation, may provide a selective advantage to hES cells in culture
2008-11-19 | GSE13565 | GEO