GEO DataSets

(Submitter supplied) RARA haploinsufficiency is an invariable consequence of t(15;17) reciprocal translocations in acute promyelocytic leukemia (APL). Furthermore, retinoids and RARA activity have been implicated in hematopoietic self-renewal, lineage commitment and neutrophil maturation. We and others therefore predicted that RARA haploinsufficiency would contribute to APL pathogenesis. To test this hypothesis we crossed RARA+/- mice with mice expressing PML-RARA from the Cathepsin G locus (mCG-PR). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6193

10 Samples

Download data: CEL

(Submitter supplied) Transcriptional profiling of murine cells expressing PML/RARA at the early promyelocyte stage (4 weeks old, preleukemic) and in full blown PML/RARA leukemia generated by transducing PML/RARA bone marrow with a Flt3-ITD retroviral vector

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL18090 GPL7202

8 Samples

Download data: TXT

(Submitter supplied) Transcriptional profiling of murine cells at the GMP, Early promyelocyte (Early Pros) and Late promyelocyte (Late Pros) stages, isolated from Wt or MRP8-PML/RARa transgenics after 2 rounds of sorting.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL18090

20 Samples

Download data: TXT

(Submitter supplied) Acute Promyelocytic Leukemia is characterized by the accumulation in the blood and bone marrow of promyelocytes. The PML/RARα fusion protein is identified as the primary abnormality implicated in the pathology, and is believed to prevent transcription of genes necessary for normal myeloid development and differentiation. Identifying its targets is critical to comprehend the road to pathogenesis. To understand how PML/RARα, in the absence of secondary lesions, alters gene expression, DNA methylation and proliferation we used a novel experimental and sorting strategy to study normal versus preleukemic promyelocytes in vivo. more...

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL13112

20 Samples

Download data: TXT

(Submitter supplied) CGH microarray in a patient with variant APL

Organism:

Homo sapiens

Type:

Genome variation profiling by genome tiling array

Platform:

GPL10123

1 Sample

Download data: TXT

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

Organism:

Mus musculus

Type:

Expression profiling by array; Genome variation profiling by genome tiling array

Platforms:

GPL11368 GPL6193

31 Samples

Download data: CEL, PAIR

(Submitter supplied) Acute Promyelocytic Leukemia (APL) is characterized by the t(15;17)(q22;q11.2) translocation, which creates a PML-RARA fusion gene that can initiate APL in mice. To discover cooperating mutations in this model, we sequenced a mouse APL genome to 15.6x haploid coverage, and discovered three somatic, non-synonymous mutations, of which one (Jak1 V657F) was recurrent. This mutation is identical to the JAK1 V658F mutation previously found in human APL and ALL samples. more...

Organism:

Mus musculus

Type:

Genome variation profiling by genome tiling array

Platform:

GPL11368

16 Samples

Download data: PAIR

(Submitter supplied) Acute Promyelocytic Leukemia (APL) is characterized by the t(15;17)(q22;q11.2) translocation, which creates a PML-RARA fusion gene that can initiate APL in mice. To discover cooperating mutations in this model, we sequenced a mouse APL genome to 15.6x haploid coverage, and discovered three somatic, non-synonymous mutations, of which one (Jak1 V657F) was recurrent. This mutation is identical to the JAK1 V658F mutation previously found in human APL and ALL samples. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6193

15 Samples

Download data: CEL

(Submitter supplied) A humanized in vivo APL model has been established utilizing the retroviral transduction of PML-RARA into human CD34+ hematopoietic cells and the transplantation of these cells into immunodeficient mice. The resultant leukemia recapitulated human APL phenotypically, and was clustered in the same category as human APL samples in the gene expression analysis.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

5 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; Other

Platforms:

GPL16791 GPL15520 GPL30173

28 Samples

Download data: NARROWPEAK

(Submitter supplied) The PML-RARA fusion protein is the hallmark driver of Acute Promyelocytic Leukemia (APL) and disrupts retinoic acid signaling, leading to wide-scale gene expression changes and uncontrolled proliferation of myeloid precursor cells. While known to be recruited to binding sites across the genome, its impact on gene regulation and expression is under-explored. Using integrated multi-omics datasets, we characterize the influence of PML-RARA binding on gene expression and regulation in an inducible cell line model and APL patient ex vivo samples. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

4 Samples

Download data: CSV

(Submitter supplied) Previous studies in our laboratory demonstrated that the azurophil granule protease neutrophil elastase (NE) cleaves PML-RARA (PR), the fusion protein that initiates acute promyelocytic leukemia (APL). Further, NE deficiency reduces the penetrance of APL in a murine model of this disease. We therefore predicted that NE-mediated PR cleavage might be important for its ability to initiate APL. To test this hypothesis, we generated a mouse expressing NE-resistant PR. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4172

Platform:

GPL570

12 Samples

Download data: CEL

Analysis of U937 cells transfected with GFP-(PML-RAR)α (PR) or GFP-PR2VR (cleavage-resistant mutant) and GFP-sorted at 6 and 9 hrs. Neutrophil elastase (NE) cleaves PR, the fusion protein that initiates acute promyelocytic leukemia. Results provide insight into leukemogenicity of NE-resistant PR.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 genotype/variation, 2 time sets

Platform:

GPL570

Series:

GSE21550

12 Samples

Download data: CEL

(Submitter supplied) The objective of the present study is to describe the gene expression of acute promyelocytic leukemia and PML/RARA oncoprotein, in a pediatric female patient, according to their clinical characteristics, immunophenotype and karyotype We used microarrays to detail the clinic and evolution of leukemia with gene expression and identified biomarkers more importan found up or down regulated genes during this process.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL23159

2 Samples

Download data: CEL, XLSX

(Submitter supplied) Acute promyelocytic leukemia (APL) is a subtype of myeloid leukemia characterized by differentiation block at the promyelocyte stage. Besides the presence of chromosomal rearrangement t(15;17) leading to formation of PML-RARA fusion, other genetic alterations have also been implicated in APL. Here, we performed comprehensive mutational analysis of primary and relapse APL to identify somatic alterations which cooperate with PML-RARA in the pathogenesis of APL. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

3 Samples

Download data: FPKM_TRACKING, TXT

(Submitter supplied) We describe a case of a child affected by a relapsed PML/RARA-negative acute promyelocytic leukemia (APL) rescued by a combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) and subsequent HSCT. We provide evidence of the presence of a chimeric viral transcript generated through genomic integration of a Torque Teno Mini Virus sequence into RARA intron 2, the recurrent breakpoint of all chimeric RARA fusions found in APL. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL18573 GPL15456

2 Samples

Download data: TXT

(Submitter supplied) Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia, that is generally driven by PML-RARA, resulting from a balanced chromosomal translocation t(15;17) (q24.1;q21.2). However, approximately 2% of APL patients carry other variants of RARA-fusions, which pose challenges for diagnosis and treatment. Here, we report a novel t(14;17) translocation in an APL patient that gave rise to a new fusion gene, STRN3-RARA. more...

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL24676 GPL24247

6 Samples

Download data: CSV

(Submitter supplied) Here we report a new fusion gene, STRN3-RARA, in acute promyelocytic leukemia (APL). It cooperates with UTX deficiency to drive full-blown APL in mice. Although STRN3-RARA leukemia quickly relapses after all-trans retinoic acid treatment, it can be restrained by cepharanthine.

Organism:

Mus musculus; Homo sapiens

Type:

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

Platforms:

GPL24247 GPL24676

22 Samples

Download data: BED, BW

(Submitter supplied) Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia, that is generally driven by PML-RARA, resulting from a balanced chromosomal translocation t(15;17) (q24.1;q21.2). However, approximately 2% of APL patients carry other variants of RARA-fusions, which pose challenges for diagnosis and treatment. Here, we report a novel t(14;17) translocation in an APL patient that gave rise to a new fusion gene, STRN3-RARA. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

12 Samples

Download data: CSV

(Submitter supplied) Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia, that is generally driven by PML-RARA, resulting from a balanced chromosomal translocation t(15;17) (q24.1;q21.2). However, approximately 2% of APL patients carry other variants of RARA-fusions, which pose challenges for diagnosis and treatment. Here, we report a novel t(14;17) translocation in an APL patient that gave rise to a new fusion gene, STRN3-RARA. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24676

4 Samples

Download data: BED, BW