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Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion [scRNA-seq]

ABSTRACT: Our preliminary data found that TNBC cells with Chrom 17p loss are more resistant to chemotherapy drug treatment, compare to cell with 17p intact.To investigate the role of cancer stemness, weg performed this gene expression profiling analysis

ORGANISM(S): Homo sapiens

PROVIDER: GSE219275 | GEO | 2022/12/10

REPOSITORIES: GEO

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Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion [RNA-seq]

Project description:Our preliminary data found that TNBC cells with Chrom 17p loss are more resistant to chemotherapy drug treatment, compare to cell with 17p intact.To investigate the role of cancer stemness, weg performed this gene expression profiling analysis

2022-12-10 | GSE219274 | GEO

Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-10 | GSE219276 | GEO

Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion

Project description:Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion

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Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion [RNA-seq]

Project description:Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion [RNA-seq]

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Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion [scRNA-seq]

Project description:Effect of Doxorubicin on gene expression of HS578T cells with or without heterozygous chromosomal 17p deletion [scRNA-seq]

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Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia

Project description:Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL. This SuperSeries is composed of the SubSeries listed below.

2008-11-11 | GSE11038 | GEO

Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia, experiment B

Project description:Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL. Keywords: genomic analysis of B-CLL with 17p loss patients

2008-11-11 | GSE11036 | GEO

Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia, experiment A

Project description:Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL. Keywords: transcriptional analysis of B-CLL with 17p loss patients

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An epigenetic mechanism underlying chromosome 17p deletion-driven tumorigenesis

Project description:Chromosome copy number variations are a hallmark of human cancers and among them chromosome 17p loss is the most common one and associated with poor prognosis. Our previous work demonstrates that 17p deletions can promote tumorigenesis more than p53 loss. Herein, with multiple functional genetic strategies, we identify a new 17p tumor suppressor, PHD finger protein 23 (PHF23). PHF23 deficiency impaires B cell differentiation and promotes Myc-driven lymphoma. Mechanistically, PHF23, a H3K4me3 reader, directly binds and represses the deacetylation activity of the SIN3-HDAC complex through its N-terminus, which coordinates two major active histone markers H3K4me3 and H3K27ac for activation of downstream B cell-differentiation genes and tumor suppressors. Further, we show that dysregulation of the PHF23-SIN3-HDAC complex is essential for PHF23 deficiency-induced tumorigenesis and maintenance. Hence, our study reveals a novel epigenetic regulatory mechanism that contributed to the pathology of 17p deleted cancers and suggests novel susceptibility of this miserable disease.

2020-12-20 | GSE145190 | GEO

Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia

2008-11-11 | E-GEOD-11038 | biostudies-arrayexpress