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Links from GEO DataSets

Items: 20

1.
Full record GDS4299

Early T-cell precursor acute lymphoblastic leukemia

Analysis of tumor cells from pediatric patients with early T-cell precursor acute lymphoblastic leukemia (ETP ALL). The ETP ALL subtype has a poor prognosis when treated with standard chemotherapy. Results provide insight into the molecular mechanisms underlying ETP ALL.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 disease state sets
Platform:
GPL13158
Series:
GSE28703
52 Samples
Download data: CEL
2.

Discovery of novel recurrent mutations and rearrangements in early T-cell precursor acute lymphoblastic leukaemia by whole genome sequencing

(Submitter supplied) Acute lymphoblastic leukaemia with early T-cell precursor immunophenotype (ETP ALL) is a highly aggressive subtype of ALL of unknown aetiology. To gain insights into the genetic basis of this disease, we performed whole genome sequencing of tumour and normal DNA of 12 children with ETP ALL. Analysis of structural and sequence variants in this discovery cohort, and mutation recurrence screening in a panel of 51 ETP and 43 non ETP ALL samples identified a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling, including IL7R, NRAS, KRAS, FLT3, BRAF, JAK1 and JAK3 in ETP ALL. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
575 Samples
Download data: CEL
Series
Accession:
GSE33315
ID:
200033315
3.

Discovery of novel recurrent mutations and rearrangements in early T-cell precursor acute lymphoblastic leukemia by whole genome sequencing

(Submitter supplied) Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole genome sequencing of tumour and normal DNA from 12 children with ETP ALL and assessed the frequency of somatic alterations in 52 ETP and 42 non-ETP T-ALL samples by sequencing and DNA copy number analysis. ETP ALL was characterised by a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF); alterations disrupting haemopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1, EP300); and inactivating mutations in histone modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4299
Platform:
GPL13158
52 Samples
Download data: CEL
Series
Accession:
GSE28703
ID:
200028703
4.

Microarray analyses of induction failure in T-ALL

(Submitter supplied) The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure. Based on the hypothesis that microarrays might identify patients who fail therapy, we used the Affymetrix U133 Plus 2.0 chip and prediction analysis of microarrays (PAM) to profile 50 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Study 9404. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL570 GPL96
92 Samples
Download data: CEL
Series
Accession:
GSE14618
ID:
200014618
5.

Microarray analyses of induction failure in T-ALL (COG study 9404)

(Submitter supplied) The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure. Based on the hypothesis that microarrays might identify patients who fail therapy, we used the Affymetrix U133 Plus 2.0 chip and prediction analysis of microarrays (PAM) to profile 50 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Study 9404. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
50 Samples
Download data: CEL
Series
Accession:
GSE14615
ID:
200014615
6.

Microarray analyses of induction failure in T-ALL (COG study 8704)

(Submitter supplied) The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure. Based on the hypothesis that microarrays might identify patients who fail therapy, we used the Affymetrix U133 Plus 2.0 chip and prediction analysis of microarrays (PAM) to profile 50 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Study 9404. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
42 Samples
Download data: CEL
Series
Accession:
GSE14613
ID:
200014613
7.

Effect of BCL11B knockdown on transcriptome of human T-cell precursors

(Submitter supplied) To investigate the role of BCL11B in the initial stages of human thymopoiesis, we performed loss of function (knockdown) studies in an in vitro human thymopoiesis model (cord blood CD34+ cells co-cultured on OP9DLL1 stromal cell line). Gene expression profiling by RNA-Seq demonstrated that BCL11B knockdown resulted in downregulation of T-lineage genes and upregulation of stem cell, myeloid and NK genes, indicating BCL11B is required for the establishment of a T-lineage commitment transcriptional program.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TXT
8.

BCL11B

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
26 Samples
Download data: TXT
Series
Accession:
GSE84678
ID:
200084678
9.

BCL11B DNA binding sites in progenitor and differentiated populations in the human thymus

(Submitter supplied) To define binding targets during thymopoiesis on a genome wide scale, we performed ChIP-Seq for BCL11B on two cell types isolated from the human thymus: the CD34+ progenitors and the more differentiated CD34- cells
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: TXT
Series
Accession:
GSE84677
ID:
200084677
10.

Effect of BCL11B overexpression on transcriptome of T-cell acute lymphoblastic leukemia (T-ALL) cells

(Submitter supplied) To investigate the effects of BCL11B on T-cell differentiation, we performed gain of function studies in cells with a T-lineage differentiation arrest, namely T-ALL cells. Gene expression profiling by RNA-Seq demonstrated that BCL11B overexpression induced transcriptional changes consistent with T-cell differentiation as early as 72 hours after transduction, indicating a rapid regulatory effect of BCL11B on the T-lineage transcriptional program and supporting an important role for BCL11B in human T-cell differentiation.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
11.

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BW, TXT
Series
Accession:
GSE76603
ID:
200076603
12.

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia (RNA-Seq)

(Submitter supplied) Purpose: To characterize transcriptional changes associated with homozygous inactivation the Polycomb Repressive Complex 2 (PRC2) lysine methyltransferase Ezh2 in a mouse model of earlt T-cell precursor ALL (ETP-ALL) Methods: We sequenced mRNA from NRASQ61K transformed murine LSK-cells co-transduced with a self-inactivating Cre-vector. Cells were sorted for Cre-expression (lox-stop-loxRosa26-YFP) or expression of an inert control vector (GFP) and differentiated on OP9DL1 stroma with and without a functional Ezh2 gene. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE76602
ID:
200076602
13.

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia (ChIP-Seq)

(Submitter supplied) Purpose: To characterize changes in genome-wide H3K27me3 associated with homozygous inactivation the Polycomb Repressive Complex 2 (PRC2) lysine methyltransferase Ezh2 in a mouse model of earlt T-cell precursor ALL (ETP-ALL) Methods: We performed Chip-seq for the H3K27me3 Chromatin mark on Ezh2ff and Ezh2ko cells NRASQ61K leukemias. Results: Inactivation of Ezh2 in this model leads to accelerated leukemia development. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: BW, TXT
Series
Accession:
GSE76601
ID:
200076601
14.

14q32 recombinations deregulating BCL11B mark a distinct Mixed Phenotype Leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing; Genome variation profiling by SNP array; SNP genotyping by SNP array
4 related Platforms
42 Samples
Download data: CEL, CYCHP, TXT
Series
Accession:
GSE162283
ID:
200162283
15.

Targeted Sequencing of BCL11B-R patients

(Submitter supplied) This study identified a cytogenetic-molecular entity, we named BCL11B-R, that showed a typical constellation of genomic features, namely BCL11B activation via chromosome translocations at 14q32, a distinct transcriptome profile, and FLT3 mutations.
Organism:
Homo sapiens
Type:
Genome variation profiling by high throughput sequencing
Platform:
GPL15520
15 Samples
Download data
Series
Accession:
GSE162282
ID:
200162282
16.

RNA-seq analysis of 12 cases with BCL11B rearrangement

(Submitter supplied) This study identified a cytogenetic-molecular entity, we named BCL11B-R, that showed a typical constellation of genomic features, namely BCL11B activation via chromosome translocations at 14q32, a distinct transcriptome profile, and FLT3 mutations.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
17.

Affymetrix SNP array data for acute leukemias with a 14q32/BCL11B rearrangement

(Submitter supplied) This study identified a cytogenetic-molecular entity, we named BCL11B-R, that showed a typical constellation of genomic features, namely BCL11B activation via chromosome translocations at 14q32, a distinct transcriptome profile, and FLT3 mutations.
Organism:
Homo sapiens
Type:
SNP genotyping by SNP array; Genome variation profiling by SNP array
Platforms:
GPL16131 GPL11157
15 Samples
Download data: CEL, CYCHP
Series
Accession:
GSE162000
ID:
200162000
18.

Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Genome variation profiling by genome tiling array; Methylation profiling by array; Other
5 related Platforms
171 Samples
Download data: HIC, IDAT, NARROWPEAK, RDS, TXT
Series
Accession:
GSE182317
ID:
200182317
19.

Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia [HiC]

(Submitter supplied) CCCTC-binding factor (CTCF) regulates the 3D chromatin architecture by facilitating chromosomal loops. In addition to insulation of euchromatin from heterochromatin, CTCF is an important transcription factor and regulator of antigen receptor and T cell receptor recombination events. CTCF inactivating events have been found in human cancer, resulting in deregulation of global gene expression by altered methylated genomic states. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL18573
8 Samples
Download data: HIC
Series
Accession:
GSE182316
ID:
200182316
20.

Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia [4C]

(Submitter supplied) CCCTC-binding factor (CTCF) regulates the 3D chromatin architecture by facilitating chromosomal loops. In addition to insulation of euchromatin from heterochromatin, CTCF is an important transcription factor and regulator of antigen receptor and T cell receptor recombination events. CTCF inactivating events have been found in human cancer, resulting in deregulation of global gene expression by altered methylated genomic states. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL18573
36 Samples
Download data: RDS
Series
Accession:
GSE182315
ID:
200182315
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