GEO DataSets

(Submitter supplied) The goals of this study are to determine whether alterations in the 3D genome organization are associated with the malignant transformation of T-ALL. We report integrated analyses of 3D genome alterations and differentially expressed genes (DEGs) in 18 newly diagnosed T-ALL patients and 4 healthy T cell controls. We found that 3D genome reorganization at the compartment, topologically associated domains (TAD), and loop levels in different subtypes of T-ALL. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other

Platform:

GPL20795

52 Samples

Download data: BEDPE, BW, H5, HIC, TXT, XLS

(Submitter supplied) Notch is needed for T cell development and is a common oncogenic driver in T cell acute lymphoblastic leukemia. Myc is a critical target of Notch in normal and malignant pre-T cells, but how Notch regulates Myc is unknown. Here, we identify a distal enhancer located >1 Mb 3' of human and murine Myc that binds Notch transcription complexes and physically interacts with the Myc proximal promoter. The Notch1 binding element in this region activates reporter genes in a Notch-dependent, cell context-specific fashion that requires a conserved Notch complex binding site. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9185

9 Samples

Download data: BED

(Submitter supplied) The main oncogenic driver in T-lymphoblastic leukemia (T-LL) is NOTCH1, which activates genes by forming chromatin-associated Notch transcription complexes. Gamma-secretase (GSI) inhibitor treatment prevents NOTCH1 nuclear localization, but most genes with NOTCH1 binding sites are insensitive to GSI. Here, we demonstrate that fewer than 10% of NOTCH1 binding sites show dynamic changes in NOTCH1 occupancy when T-LL cells are toggled between the Notch-on and –off states with GSI. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

15 Samples

Download data: BED

(Submitter supplied) Mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes are frequently observed in a wide variety of hematologic malignancies, including myeloid and T-cell leukemias. In this study, we generated Idh2R140Q transgenic mice to examine the role of the Idh2R140Q mutation in leukemia. No leukemia developed in Idh2R140Q transgenic mice, suggesting a need for additional genetic events for leukemia development. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

18 Samples

Download data: CEL, XLSX

(Submitter supplied) To dissect molecular pathways regulated by TRIB2 in T-ALL, we performed microarray gene expression profiling in the TAL1-positive T-ALL cells (Jurkat) after TRIB2 knockdown.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

4 Samples

Download data: CEL

(Submitter supplied) The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, GATA3, ETS1 and RUNX1 in T-ALL cells. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

22 Samples

Download data: WIG, YLF

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL11154 GPL13232 GPL9115

64 Samples

Download data: CEL, WIG, YLF

(Submitter supplied) The oncogenic transcription factor TAL1/SCL is aberrantly expressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing its importance in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, LMO1, LMO2, GATA3 and RUNX1 in T-ALL cells. We show that TAL1 forms an interconnected auto-regulatory loop with its partners, and that the TAL1 complex directly activates the MYB oncogene, forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9115

10 Samples

Download data: WIG, YLF

(Submitter supplied) The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, GATA3, ETS1 and RUNX1 in T-ALL cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13232

32 Samples

Download data: CEL

(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

14 Samples

Download data: BED, BW

(Submitter supplied) ChIP-sequencing samples to improve our understanding of how genes are activated or repressed in healthy and diseased human cells.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

2 Samples

Download data: BED, BW

(Submitter supplied) ChIP-sequencing samples to improve our understanding of how genes are activated or repressed in healthy and diseased human cells.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

3 Samples

Download data: BED, BW

(Submitter supplied) RNA-sequencing samples to improve our understanding of gene expression and gene expression changes between healthy and diseased leukemic primary samples.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

9 Samples

Download data: BW, TSV

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) cells represent developmentally arrested T-cell progenitors, subsets of which aberrantly express homeobox genes of the NKL subclass, including TLX1, TLX3, NKX2-1, NKX2-5, NKX3-1 and MSX1. Here, we analyzed the transcriptional landscape of all 48 members of the NKL homeobox gene subclass in CD34+ hematopoietic stem cells (HSCs) and during lymphopoiesis, identifying activities of 9 particular genes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

11 Samples

Download data: CEL

(Submitter supplied) We used microarrays to detail the global program of gene expression underlying stemness of hematopoietic cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

1 Sample

Download data

(Submitter supplied) The NUP214-ABL1 fusion is a constitutively activated tyrosine kinase that is significantly associated with overexpression of the TLX1 or TLX3 transcription factors in T-cell acute lymphoblastic (T-ALL). Here we show that NUP214-ABL1 kinase cooperates with TLX1 in driving T-ALL development using a transgenic mouse model. Using ChIP-seq and ATAC-seq, we show that TLX1 and STAT5, the downstream effector of NUP214-ABL1, selectively increase the accessibility of enhancer regions, and cooperatively activate the expression of key proto-oncogenes such as MYC and BCL2. more...

Organism:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL17021 GPL16791

69 Samples

Download data: BEDGRAPH, NARROWPEAK, TXT

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner possibly delineating specific T-ALL subgroups. One subgroup, including MLL-rearranged, CALM-AF10 or inv(7)(p15q34) cases, is characterized by elevated expression of HOXA genes. Using a gene expression based clustering analysis of 67 T-ALL cases with recurrent molecular genetic abnormalities and 25 samples lacking apparent aberrations, we identified 5 new cases with elevated HOXA levels. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

92 Samples

Download data: CEL

(Submitter supplied) Lymphoblastic lymphoma (LBL) is one of the most frequent occurring pediatric non-Hodgkin lymphomas. In the WHO classification scheme pediatric LBL is considered to be the same disease entity as pediatric acute lymphoblastic leukemia (ALL). However, it is unclear whether the genetic basis of pediatric LBL development is similar to that of pediatric ALL. We performed genome-wide analyses of copy number aberrations in 12 T-LBL and 7 precursor B-cell LBL pediatric cases using high-resolution SNP-based array CGH. more...

Organism:

Homo sapiens

Type:

Genome variation profiling by SNP array; SNP genotyping by SNP array

Platform:

GPL3718

25 Samples

Download data: CEL, CHP

(Submitter supplied) T-cell Acute Lymphoblastic Leukaemia (T-ALL) can be classified into a number of subfamilies, including those that overexpress TAL1/LMO, TLX1/3 and HOXA transcription factors. Whilst it has been previously shown in mouse models that TAL1/LMO transcription factors induce thymocyte self-renewal, whether this is the case for other transcription factor subclasses is currently unknown. To address this, we have studied vav-Nup98-HoxD13-transgenic (NHD13-Tg) mice, a model of HOXA-driven T-ALL, which overexpress HOXA transcription factors throughout haematopoiesis and display features of myelodysplastic syndrome in the bone marrow along with T-cell developmental abnormalities in the thymus and subsequent development of T-ALL in approximately 15% of mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6887

12 Samples

Download data: TXT

(Submitter supplied) We performed ChIP-on-chip analysis of primary ATL patient cells, normal CD4+ T cells, and Tax-transduced cells to decipher the ATL-specific ‘epigenetic-code’ that was critical in ATL pathogenesis.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by genome tiling array

Platform:

GPL19784

17 Samples

Download data: TXT