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Links from GEO DataSets

Items: 18

1.

Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2 [epitranscriptome]

(Submitter supplied) Myelodysplastic syndrome (MDS) is a clonal myeloid neoplasm characterized by ineffective haematopoiesis and cytopenia with frequent epigenetic modifications. Hypomethylating agents (HMA) such as azacitidine (AZA) and decitabine (DEC) are standard therapeutic options in MDS, but drug resistance is not uncommon.To study RNA modification in particular M6A, P39-AZA-S and P39-AZA-R native RNA libraries were prepared using the direct RNA sequencing kit (Oxford Nanopore) following the manufacturer’s protocol (SQK-RNA002). more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL28975
2 Samples
Download data: TXT
Series
Accession:
GSE165064
ID:
200165064
2.

Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing; Methylation profiling by genome tiling array; Expression profiling by high throughput sequencing
Platforms:
GPL21145 GPL28975 GPL23227
10 Samples
Download data: IDAT
Series
Accession:
GSE165188
ID:
200165188
3.

Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2 [transcriptome]

(Submitter supplied) Myelodysplastic syndrome (MDS) is a clonal myeloid neoplasm characterized by ineffective haematopoiesis and cytopenia with frequent epigenetic modifications. Hypomethylating agents (HMA) such as azacitidine (AZA) and decitabine (DEC) are standard therapeutic options in MDS, but drug resistance is not uncommon. Herein, multi-omic analysis is used to identify signaling pathways during MDS HMA resistance using MDS cell line P39 and validated in P39 and Kasumi-1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23227
4 Samples
Download data: TXT
4.

Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2 [methylome]

(Submitter supplied) Myelodysplastic syndrome (MDS) is a clonal myeloid neoplasm characterized by ineffective haematopoiesis and cytopenia with frequent epigenetic modifications. Hypomethylating agents (HMA) such as azacitidine (AZA) and decitabine (DEC) are standard therapeutic options in MDS, but drug resistance is not uncommon. Herein, multi-omic analysis is used to identify signaling pathways during MDS HMA resistance using MDS cell line P39 and validated in P39 and Kasumi-1. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
4 Samples
Download data: IDAT, TXT
Series
Accession:
GSE165185
ID:
200165185
5.

A methylation signature at diagnosis in patients with high-risk Myelodysplastic Syndromes and secondary Acute Myeloid Leukemia predicts azacitidine response but not relapse

(Submitter supplied) Epigenetic therapy, using hypomethylating agents (HMA), is known to be effective in the treatment of high-risk myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients who are not suitable for intensive chemotherapy or allogeneic stem cell transplantation. However, response rates to HMA are low and there is an unmet need in finding prognostic and predictive biomarkers of treatment response. more...
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL13534
166 Samples
Download data: IDAT, TSV
Series
Accession:
GSE152710
ID:
200152710
6.

Transcriptome profiling by RNA-sequencing of the AML cell lines UCSD-AML1 and ELF-153.

(Submitter supplied) DNMT inhibitors (DNMTi) are finally approved for AML/MDS, also based on their activity in patients with high-risk cytogenetics (often monosomal karyotype) such as -5/del(5q) or -7/del(7q), often - but not always - harboring TP53-mutations. Several studies provided evidence for aberrant hypermethylation/silencing on monoallelic gene loci, including tumor suppressor genes. We hypothesized that transcriptional repression on monosomal gene loci may be preferentially reversed by DNMTi. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
24 Samples
Download data: TXT
Series
Accession:
GSE140347
ID:
200140347
7.

Gene expression data of serially sorted primary AML patient blasts prior and after treatment with the DNMT inhibitor decitabine (DAC)

(Submitter supplied) DNMT inhibitors (DNMTi) are finally approved for AML/MDS, also based on their activity in patients with high-risk cytogenetics (often monosomal karyotype) such as -5/del(5q) or -7/del(7q), often - but not always - harboring TP53-mutations. Several studies provided evidence for aberrant hypermethylation/silencing on monoallelic gene loci, including tumor suppressor genes. We hypothesized that transcriptional repression on monosomal gene loci may be preferentially reversed by DNMTi. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
80 Samples
Download data: CEL
Series
Accession:
GSE138696
ID:
200138696
8.

Copy-number profiling by SNP array of 4 acute myeloid leukemia (AML) cell lines

(Submitter supplied) DNMT inhibitors (DNMTi) are finally approved for AML/MDS, also based on their activity in patients with high-risk cytogenetics (often monosomal karyotype) such as -5/del(5q) or -7/del(7q), often - but not always - harboring TP53-mutations. Several studies provided evidence for aberrant hypermethylation/silencing on monoallelic gene loci, including tumor suppressor genes. We hypothesized that transcriptional repression on monosomal gene loci may be preferentially reversed by DNMTi. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array
Platforms:
GPL18637 GPL6801
4 Samples
Download data: CEL, CNCHP, CYCHP
Series
Accession:
GSE138438
ID:
200138438
9.

miRNA expression profiling in a murine model of KrasG12D induced CMML-like MPD

(Submitter supplied) Mx1-Cre/KrasG12D mice were injected with pIpC to induce a myeloproliferative disease resembling human chronic myelomonocytic leukemia (CMML-like MPD). When the disease was fully developed, CD11b-/Ly6G-/c-Kit+ hematopoietic stem and progenitor cells (HSPCs) were isolated and subjected to miR-microarray expression profiling. pIpC-injected CD11b-/Ly6G-/c-Kit+ HSPCs of age matched wildytpe control mice were used as controls.
Organism:
synthetic construct; Mus musculus
Type:
Non-coding RNA profiling by array
Platform:
GPL19117
8 Samples
Download data: CEL
Series
Accession:
GSE145083
ID:
200145083
10.

Mitotic perturbation is a key mechanism of action of decitabine in myeloid tumor treatment II

(Submitter supplied) Decitabine (DAC) is used clinically for myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Our genome-wide CRISPR-dCas9 activation screen using MDS-derived AML cells shows that mitotic regulation plays a pivotal role in DAC resistance. DAC strongly induces abnormal mitosis (abscission failure or tripolar mitosis) in human myeloid tumors at clinical concentrations, especially in those with TP53 mutations and antecedent hematological disorders. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL17021
4 Samples
Download data: TXT
Series
Accession:
GSE240570
ID:
200240570
11.

Mitotic perturbation is a key mechanism of action of decitabine in myeloid tumor treatment

(Submitter supplied) Decitabine (DAC) is used clinically for myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). To elucidate its exact mechanism of action, we performed a genome-wide CRISPR-dCas9 activation screen using MDS-derived AML cells and revealed that mitotic regulation plays a pivotal role in DAC resistance. DAC strongly induces abnormal mitosis (abscission failure or tripolar mitosis) in human myeloid tumors at clinical concentrations, especially in those with TP53 mutations and antecedent hematological disorders. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
Series
Accession:
GSE240439
ID:
200240439
12.

Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

(Submitter supplied) 5-Aza-2'-deoxycytidine, also known as decitabine, is a DNA hypomethylating agent (HMA) used to treat acute myeloid leukemia (AML) and pre-leukemic disorder myelodysplastic syndrome (MDS). Decitabine activates the transcription of endogenous retroviruses (ERV), which can induce immune response by acting as cellular double-stranded RNAs. Here, we employ an image-based screening system to identify dsRNA-binding factors that mediate the downstream effect of ERV induction. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
11 Samples
Download data: TXT
13.

Analysis of genome-wide methylation and gene expression induced by decitabine treatment in HL60 leukemia cell line

(Submitter supplied) Epigenetic changes play a role in the pathogenesis of myeloid malignancies and hypomethylating agents have shown efficacy in these diseases. We studied the apoptotic effect, the genome-wide methylation and gene expression profiles in HL60 cells following decitabine treatment, using micro-array technologies. Decitabine treatment resulted in a decrease in global DNA methylation, corresponding to 4876 probeset IDs with significantly reduced methylation levels, while expression of 2583 IDs was induced. more...
Organism:
Homo sapiens
Type:
Expression profiling by array; Methylation profiling by genome tiling array
Platforms:
GPL570 GPL5082
12 Samples
Download data: CEL, TXT
Series
Accession:
GSE24224
ID:
200024224
14.

Preclinical efficacy of azacitidine and venetoclax for infant KMT2A-rearranged ALL reveals a new therapeutic strategy

(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 genome tiling array
Platforms:
GPL24676 GPL21145
78 Samples
Download data: IDAT
Series
Accession:
GSE212592
ID:
200212592
15.

Transcriptomic profiling of KMT2A-rearranged infant acute lymphoblastic leukemia (ALL) cells after treatment witith azacitidine and decitabine.

(Submitter supplied) Transcriptomic profiling was performed on six cell lines derived from infants with KMT2A-rearranged ALL following treatment with two hypomethylating drugs (azacitidine and decitabine) administered at low doses for 72 hours in vitro. We identified changes in gene expression following treatment with hypomethylating agents, with decitabine exerting a greater effect than azacitidine.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
54 Samples
Download data: TXT
Series
Accession:
GSE212591
ID:
200212591
16.

Genome-wide methylation profiling of KMT2A-rearranged infant Acute Lymphoblastic Leukemia (ALL) cells after treatment with azacitidine, decitabine and zebularine

(Submitter supplied) Genome-wide methylation profiling was performed on six cell lines derived from infants with KMT2A-rearranged ALL following treatment with three hypomethylating drugs (azacitidine, decitabine and zebularine) administered at low doses for 72 hours in vitro. We identified drug-specific and common differentially methylated regions and validated differentially expressed genes located within such regions, indicating commonalities in pathways targeted by azacitidine and decitabine in KMT2A-rearranged infant ALL. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
24 Samples
Download data: IDAT
Series
Accession:
GSE198679
ID:
200198679
17.

Immunologic predictors for clinical responses during immune checkpoint blockade in patients with myelodysplastic syndromes

(Submitter supplied) We investigated the immune-related gene expression signature in the tumor immune-microenvironment associated with response or resistance during immunotherapy, by performing targeted gene expression profiling and gene set enrichment analysis using a custom NanoString panel composed of 579 immune-related genes
Organism:
Homo sapiens
Type:
Other
Platform:
GPL31171
98 Samples
Download data: RCC
Series
Accession:
GSE219085
ID:
200219085
18.

Investigating microenvironment in MDS

(Submitter supplied) High BM plasma S100A8/A9 is associated with a perturbed microenvironment and poor prognosis in myelodysplastic syndromes
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
215 Samples
Download data: CSV
Series
Accession:
GSE223305
ID:
200223305
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