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accession-icon GSE80000
Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Sample Metadata Fields

Sex

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accession-icon GSE79999
Adam17-Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling (macrophage)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Gene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice.

Publication Title

Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Sample Metadata Fields

Sex

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accession-icon GSE79998
Adam17-Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling (aorta)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Gene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice.

Publication Title

Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Sample Metadata Fields

Sex

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accession-icon GSE15434
Gene expression profiling in AML with normal karyotype: A multicenter study investigating molecular markers in 251 cases
  • organism-icon Homo sapiens
  • sample-icon 251 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Acute myeloid leukemia (AML) is a heterogeneous disease and AML with normal karyotype (AML-NK) is categorized as an intermediate-risk group. Over the past years molecular analyses successfully identified biomarkers that will further allow to dissecting clinically meaningful subgroups in this disease. Thus far, somatic mutations were identified which elucidate the disturbance of cellular growth, proliferation, and differentiation processes in hematopoietic progenitor cells. In AML-NK, acquired gene mutations with prognostic relevance were identified for FLT3, CEBPA, and NPM1. FLT3-ITD mutations were associated with short relapse-free and overall survival, while mutations in CEBPA or NPM1 (without concomitant FLT3-ITD) had a more favorable outcome.

Publication Title

Quantitative comparison of microarray experiments with published leukemia related gene expression signatures.

Sample Metadata Fields

Sex, Age, Disease, Disease stage

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accession-icon GSE7757
Robustness of gene expression signatures in leukemia: comparison of three distinct total RNA preparation procedures.
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarray gene expression (MAGE) signatures allow insights into the transcriptional processes of leukemias and may evolve as a molecular diagnostic test. Introduction of MAGE into clinical practice of leukemia diagnosis will require comprehensive assessment of variation due to the methodologies.

Publication Title

New data on robustness of gene expression signatures in leukemia: comparison of three distinct total RNA preparation procedures.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39671
Expression data from untreated CLL patients
  • organism-icon Homo sapiens
  • sample-icon 124 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The clinical course of patients with chronic lymphocytic leukemia (CLL) is heterogeneous. Several prognostic factors have been identified that can stratify patients into groups that differ in their relative tendency for disease progression and/or survival. Here, we pursued a subnetwork-based analysis of gene expression profiles to discriminate between groups of patients with disparate risks for CLL progression.

Publication Title

Subnetwork-based analysis of chronic lymphocytic leukemia identifies pathways that associate with disease progression.

Sample Metadata Fields

Specimen part

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accession-icon SRP092412
B cell differentiation is limited by de novo DNA methylation [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

B cells provide humoral immunity by differentiating into antibody-secreting plasma cells, a process that requires cell division and is linked to DNA hypomethylation and gene regulation. Conversely, accumulation of DNA methylation in B cell differentiation is less apparent. To determine the role of de novo DNA methylation in B cell differentiation, the de novo DNA methyltransferases, Dnmt3a and Dnmt3b, were deleted in B cells resulting in phenotypically normal B cell development in the bone marrow, spleen and lymph nodes. However, upon immunologic challenge, mice deficient for Dnmt3a and Dnmt3b (Dnmt3-deficient) accumulated more antigen-specific B cells and bone marrow chimeras showed this was cell-autonomous. Additionally, a five-fold increase in splenic and bone marrow plasma cells was observed. Molecular analysis revealed that Dnmt3-deficient bone marrow plasma cells failed to repress gene expression to the same level as their Dnmt3ab-sufficient counterparts. This was coupled with a failure of Dnmt3-deficient germinal center B cells and plasma cells to gain and/or maintain DNA methylation at several thousand loci that were clustered in enhancers of genes that function in B cell activation and homing. Analysis of chromatin accessibility showed Dnmt3-deficient plasma cells had increased accessibility at several genes involved in hematopoiesis and B cell differentiation. These data show that de novo DNA methylation limits B cell activation, proliferation and differentiation, and support a model whereby DNA methylation represses the aberrant transcription of genes silenced in B cell differentiation to maintain plasma cell homeostasis. Overall design: Naïve lymph node B cells (B220+ GL7- Fas-), Phycoerythrin-specific germinal center B cells (B220+ GL7+ Fas+ PE+), and bone marrow plasma cells (CD138+) were compared between Cd19cre/wtDnmt3afl/flDnmt3bfl/fl (Dnmt3-deficient) and littermate control Cd19wt/wtDnmt3afl/flDnmt3bfl/fl (Dnmt3-sufficient) mice using RRBS, RNA-seq, and ATAC-seq. Naïve lymph node B cells were taken from naïve mice, whereas PE-specific germinal center B cells and bone marrow plasma cells were isolated from mice that had been immunized with phycoerythrin 30 days prior. This Series includes the RNA-seq component of the study.

Publication Title

B cell activation and plasma cell differentiation are inhibited by de novo DNA methylation.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE34733
Methylation of the Proximal, Distal and Core Promoter of CEBPA in 572 Cases with Normal Karyotpye AML and 44 with t(8;21) Disclosed Different Frequencies but no Impact on Prognosis
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The clinical impact of aberrant CEBPA promoter methylation (PM) in AML is controversial discussed. The aim of this study was to clarify the significance of aberrant CEBPA PM with regard to clinical features in a cohort of 572 de novo AML with wildtype CEBPA and normal karyotype. The distal promoter was methylated in 54/572 cases (9.41%) whereas proximal PM was never detected. Methylation of the core promoter was detected in only 8 of 326 cases (2.45%) and thus seems to be a rare event in AML. There was no correlation between CEBPA distal PM, age, sex, white blood cell (WBC) count or Hb levels at diagnosis. We also were not able to detect a significant correlation between the presence of CEBPA distal PM and molecular mutations such as FLT3-ITD, NPM1, AML1, MLL-PTD and IDH1. Solely the frequency of IDH2R140 mutations was significantly reduced in CEBPA distal PM positive compared to CEBPA distal PM negative cases (p=0.01). Furthermore, analysis of CEBPA mRNA expression level revealed no difference between CEBPA distal PM positive and CEBPA distal PM negative cases, suggesting that CEBPA distal PM has no influence on CEBPA expression. CEBPA distal PM did not show impact on overall survival (OS), event free survival (EFS) or incidence of relapse. Also when other mutations were taken into regard no prognostic impact of CEBPA distal PM could be shown. In contrast, a distinct expression profile of CEBPA distal PM positive cases compared to CEBPA mutated and CEBPA distal PM negative cases was observed. In addition, a significantly higher frequency of CEBPA distal PM was detected in RUNX1-RUNX1T1 positive AML compared to the CEBPA witdtype cases. We conclude that the presence of aberrant CEBPA PM has no clinical relevance and is therefore a negligible prognostic marker in de novo AML with normal karyotype.

Publication Title

Frequency and prognostic impact of CEBPA proximal, distal and core promoter methylation in normal karyotype AML: a study on 623 cases.

Sample Metadata Fields

Disease

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accession-icon GSE15061
Gene array prediction of AML transformation in MDS
  • organism-icon Homo sapiens
  • sample-icon 431 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarray-based classifiers and prognosis models identify subgroups with distinct clinical outcomes and high risk of AML transformation of myelodysplastic syndrome (MDS)

Publication Title

Microarray-based classifiers and prognosis models identify subgroups with distinct clinical outcomes and high risk of AML transformation of myelodysplastic syndrome.

Sample Metadata Fields

Disease, Disease stage

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accession-icon GSE21261
Multilineage Dysplasia (MLD) in AML correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance
  • organism-icon Homo sapiens
  • sample-icon 85 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Full Title: Multilineage Dysplasia (MLD) in AML correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: A comparison of 408 cases classified as AML not otherwise specified or AML with myelodysplasia-related changes

Publication Title

Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC).

Sample Metadata Fields

No sample metadata fields

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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