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Links from GEO DataSets

Items: 20

1.

Next gen RNA sequencing of mouse acute myeloid leukemia

(Submitter supplied) Trascriptome analysis of aml samples were performed
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
9 Samples
Download data: TXT
Series
Accession:
GSE87870
ID:
200087870
2.

Leukemia stem cell-enriched population expresses self-renewal gene-expression signature [RNA-Seq]

(Submitter supplied) Mutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
24 Samples
Download data: TXT
Series
Accession:
GSE63312
ID:
200063312
3.

NRASG12V oncogene mediates self-renewal in acute myelogenous leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL1261 GPL13112
55 Samples
Download data: CEL
Series
Accession:
GSE49089
ID:
200049089
4.

NRASG12V mediates leukemia self renewal [RNA-Seq]

(Submitter supplied) Mutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE49088
ID:
200049088
5.

NRASG12V mediates self renewal in AML [RNA-Seq]

(Submitter supplied) Mutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE49087
ID:
200049087
6.

NRASG12V mediates leukemia self renewal [Microarray]

(Submitter supplied) Mutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
15 Samples
Download data: CEL
Series
Accession:
GSE49038
ID:
200049038
7.

TNFAIP8 promotes AML chemoresistance by activating ERK signaling pathway through interaction with Rac1

(Submitter supplied) The tumor necrosis factor induced protein 8 (TNFAIP8), a novel anti-apoptotic molecule, has been implicated in chemoresistance of several types of neoplasms, but its role in AML remains to be elucidated. In this study, upregulated TNFAIP8 expression was found in human AML patients and cell lines. E74 like ETS transcription factor 1 (ELF1) was identified to contribute to its aberrant expression. Forced expression of TNFAIP8 protected cells from apoptosis induced by chemotherapeutic agents and increased drug resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
8.

Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL17021
27 Samples
Download data: TXT
Series
Accession:
GSE96761
ID:
200096761
9.

Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity [bisulfite-Seq]

(Submitter supplied) Recent studies using next-generation sequencing technology have uncovered mutational landscapes of various myeloid malignancies (Cancer Genome Atlas Research Network, 2013; Yoshida et al., 2011). These genetic data revealed novel classes of mutations that commonly occur in patients with myeloid malignancies, including epigenetic regulators and spliceosomal genes. In addition, co-occurrence and mutual exclusivity of these disease alleles suggest convergent cooperative roles or common biological effects of specific alleles in myeloid leukemogenesis (Shih et al., 2012). more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE96759
ID:
200096759
10.

Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity [RNA-Seq]

(Submitter supplied) Recent studies using next-generation sequencing technology have uncovered mutational landscapes of various myeloid malignancies (Cancer Genome Atlas Research Network, 2013; Yoshida et al., 2011). These genetic data revealed novel classes of mutations that commonly occur in patients with myeloid malignancies, including epigenetic regulators and spliceosomal genes. In addition, co-occurrence and mutual exclusivity of these disease alleles suggest convergent cooperative roles or common biological effects of specific alleles in myeloid leukemogenesis (Shih et al., 2012). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
15 Samples
Download data: TXT
Series
Accession:
GSE96758
ID:
200096758
11.

A gain-of-function p53 mutant synergizes with oncogenic Nras to promote acute myeloid leukemia in mice

(Submitter supplied) We previously demonstrated that a subset of acute myeloid leukemia (AML) patients with concurrent RAS pathway and TP53 mutations have extremely poor prognosis, and most of these TP53 mutations are missense mutations. Here, we report that in contrast to mixed AML and T-cell malignancy developed in NrasG12D/+; p53-/- (NP-/-) mice, NrasG12D/+; p53R172H/+ (NPmut) mice rapidly developed an inflammation-associated AML. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
13 Samples
Download data: CSV
Series
Accession:
GSE243642
ID:
200243642
12.

Assessment of MEK-ERK pathway targeting by BRAF, NRAS and KRAS gene mutations in plasma cell dyscrasias

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19824
146 Samples
Download data: CEL
Series
Accession:
GSE66293
ID:
200066293
13.

Assessment of MEK-ERK pathway targeting by BRAF, NRAS and KRAS gene mutations in plasma cell dyscrasias [U266 human myeloma cell line]

(Submitter supplied) Multiple myeloma (MM) is a malignant disorder characterized by the clonal proliferation of plasma cells (PCs) in the bone marrow (BM). The genetic background and clinical course of the disease are largely heterogeneous, and MM pathophysiology ranges from the premalignant condition of monoclonal gammopathy of undetermined significance (MGUS) to smoldering MM, symptomatic MM, and extramedullary MM/plasma cell leukemia (PCL). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19824
4 Samples
Download data: CEL
Series
Accession:
GSE66292
ID:
200066292
14.

Assessment of MEK-ERK pathway targeting by BRAF, NRAS and KRAS gene mutations in plasma cell dyscrasias [Patient samples]

(Submitter supplied) Multiple myeloma (MM) is a malignant disorder characterized by the clonal proliferation of plasma cells (PCs) in the bone marrow (BM). The genetic background and clinical course of the disease are largely heterogeneous, and MM pathophysiology ranges from the premalignant condition of monoclonal gammopathy of undetermined significance (MGUS) to smoldering MM, symptomatic MM, and extramedullary MM/plasma cell leukemia (PCL). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19824
142 Samples
Download data: CEL
Series
Accession:
GSE66291
ID:
200066291
15.

B11 cells created by replacing the NRAS-G12D mutation in THP1 cells with a dox-inducible NRAS-G12V mutation

(Submitter supplied) To study the role of NRAS mutations in cell proliferation and self-renewal in acute myeloid leukemia (AML), the human AML cell line, THP1, was modified to replace its naturally occurring heterozygous NRAS-G12D mutation with a doxycycline(dox)-inducible heterozygous NRAS-G12V mutation. The endogenous copies of the NRAS-G12D allele were deleted using CRISPR/Cas9 after a dox-inducible, CRISPR resistant, NRAS-G12V transgene was introduced into the THP1 cell line. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: TXT
16.

Wild-Type Nras Lacks Tumor Suppressor Activity and Nras Oncogene Dosage Strongly Modulates Hematopoietic Transformation

(Submitter supplied) Contemporary treatment of pediatric acute myeloid leukemia (AML) requires the assignment of patients to specific risk groups. To explore whether expression profiling of leukemic blasts could accurately distinguish between the known risk groups of AML, we analyzed 130 pediatric and 20 adult AML diagnostic bone marrow or peripheral blood samples using the Affymetrix U133A microarray. Class discriminating genes were identified for each of the major prognostic subtypes of pediatric AML, including t(15;17)[PML-RARalpha], t(8;21)[AML1-ETO], inv(16) [CBFbeta-MYH11], MLL chimeric fusion genes, and cases classified as FAB-M7. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
108 Samples
Download data: CEL
Series
Accession:
GSE43176
ID:
200043176
17.

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
18.

Mutant SETBP1 enhances NRAS-driven MAPK pathway activation to promote aggressive leukemia

(Submitter supplied) Mutations in SET binding protein 1 (SETBP1) are associated with poor outcomes in myeloid leukemias. In the Ras-driven leukemia, juvenile myelomonocytic leukemia, SETBP1 mutations are enriched in relapsed disease. We demonstrate that SETBP1 enhances the NRAS gene expression signature, driving upregulation of mitogen-activated protein kinase (MAPK) signaling and downregulation of differentiation pathways.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE158379
ID:
200158379
19.

Expression data from second oncogene expressing Melanoma Cells.

(Submitter supplied) Among the myriad tumors analyzed to date, cutaneous malignant melanomas bear some of the highest mutational burdens. Thus, it is somewhat surprising that oncogene exclusion between is so pronounced in melanomas where there is only a single melanoma out of 366 sequenced specimens which harbors concurrent BRAF(V600E/M) and NRAS(G13R) mutations (TCGA-ES-A2NC Sample; WWW.bioportal.org), In this senario some NRAS and BRAF mutations co-expressing cells show slow growth phenotypes by under study mechanism. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16043
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE122835
ID:
200122835
20.

Analysis of SKMEL-103, AsPC1 and RH-36 cells after treatment with BAY 11-7082

(Submitter supplied) To identify the gene expression changes in NRAS mutant cell line SKMEL-103, KRAS mutant cell line AsPC1 and HRAS mutant cell line RH-36 upon BAY 11-7082 treatment, we analyzed these cell line with either control DMSO or BAY 11-7082 treatment via RNA sequencing.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: TXT
Series
Accession:
GSE251968
ID:
200251968
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