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accession-icon GSE15695
Comprehensive Homozygous Deletion Mapping of Myeloma Defines a Poor Prognosis Cell Death Gene Expression Signature
  • organism-icon Homo sapiens
  • sample-icon 244 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Myeloma is a clonal malignancy of plasma cells. Poor prognosis risk is currently identified by clinical and cytogenetic features. However, these indicators do not capture all prognostic information. Gene expression analysis can be used to identify poor prognosis patients and this can be improved by combination with information about DNA level changes. Using SNP-based gene mapping in combination with global gene expression analysis we have identified homozygous deletions in genes and networks that are relevant to myeloma. From these, we have generated an expression-based signature associated with shorter survival in 247 patients and confirmed this signature in data from 2 independent groups totalling 800 patients. We identified 170 genes with homozygous deletions and corresponding loss of expression. Deletion within the Cell Death network was over-represented and cases with these deletions have impaired overall survival. We defined a gene expression signature of 97 cell death genes that reflects prognosis confirmed this in two independent data sets. We developed a simple 6-gene expression signature from the 97-gene signature that can be used to identify poor prognosis myeloma in the clinical environment. The signature can form the basis of future trials aimed at improving the outcome of poor prognosis myeloma.

Publication Title

Homozygous deletion mapping in myeloma samples identifies genes and an expression signature relevant to pathogenesis and outcome.

Sample Metadata Fields

Specimen part

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accession-icon GSE48591
Runx3 regulated genes in splenic CD4+ dendritic cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional reprogramming of CD11b+Esam(hi) dendritic cell identity and function by loss of Runx3.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE45374
Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cell-autonomous function of Runx1 transcriptionally regulates mouse megakaryocytic maturation.

Sample Metadata Fields

Specimen part

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accession-icon GSE45373
Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice (expression)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

RUNX1 transcription factor (TF) is a key regulator of megakaryocytic development and when mutated is associated with familial platelet disorder and predisposition to acute myeloid leukemia (FPD-AML). We used mice lacking Runx1 specifically in megakaryocytes (MKs) to characterize the Runx1-mediated transcriptional program during advanced stages of MK differentiation. Gene expression and chromatin-immunoprecipitation-sequencing (ChIP-seq) of Runx1 andp300identified functional Runx1-bound MK enhancers. Runx1/p300 co-bound regions showed significant enrichment in genes important for MK and platelet homeostasis. Runx1-bound regions were highly enriched in RUNX and ETS motifs and to a lesser extent in GATA motif.The data providesthe first example of genome-wide Runx1/p300 occupancy in maturating FL-MK,unravels the Runx1-regulated program controlling MK maturationin vivoandidentifies itsbona fideregulated genes. It advances our understandingof the molecular events that upon mutations in RUNX1 lead to thepredisposition to familial platelet disorders and FPD-AML.

Publication Title

Cell-autonomous function of Runx1 transcriptionally regulates mouse megakaryocytic maturation.

Sample Metadata Fields

Specimen part

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accession-icon GSE48589
Runx3 function in CD4+ splenic dendritic cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CD4+ dendritic cells are part of the innate immunity essential for priming and activating of CD4+ T cells

Publication Title

Transcriptional reprogramming of CD11b+Esam(hi) dendritic cell identity and function by loss of Runx3.

Sample Metadata Fields

Sex, Age

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accession-icon GSE48590
The affect of specific ablation of Runx3 from Esam splenic dendritic cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Esam/CD4+ dendritic cells are part of the innate immunity essential for priming and activating of CD4+ T cells

Publication Title

Transcriptional reprogramming of CD11b+Esam(hi) dendritic cell identity and function by loss of Runx3.

Sample Metadata Fields

Sex, Age

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accession-icon GSE136067
Runx3 prevents spontaneous colitis by directing differentiation of anti-inflammatory mononuclear phagocytes
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Runx3 prevents spontaneous colitis by directing the differentiation of anti-inflammatory mononuclear phagocytes.

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon GSE136066
Runx3 function in colon resident macrophages (RM) and CD11b+ dendritic cells (DC).
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

RUNX3 is one of three mammalian Runt-domain transcription factors that regulate gene expression in several types of immune cells. Runx3-deficiency in mice is associated with a multitude of defects in the adaptive and innate immunity systems, including the development of early onset colitis. Our study reveals that conditional deletion of Runx3 specifically in mononuclear phagocytes (MNP) recapitulates the early onset spontaneous colitis seen in Runx3-/- mice. We show that Runx3 is expressed in colonic MNP, including RM and the dendritic cell cDC2 subsets and its loss results in impaired differentiation/maturation of both cell types.

Publication Title

Runx3 prevents spontaneous colitis by directing the differentiation of anti-inflammatory mononuclear phagocytes.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP057984
Akt1/Protein Kinase B Enhances Transcriptional Reprogramming of Fibroblasts to Functional Cardiomyocytes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Conversion of fibroblasts to functional cardiomyocytes represents a potential approach for restoring cardiac function following myocardial injury, but the technique thus far has been slow and inefficient. To improve the efficiency of reprogramming fibroblasts to cardiac-like myocytes (iCMs) by cardiac transcription factors (Gata4, Hand2, Mef2c, and Tbx5=GHMT), we screened 192 protein kinases and discovered that Akt/protein kinase B dramatically accelerates and amplifies this process. Approximately 50% of reprogrammed fibroblasts displayed spontaneous beating after three weeks of induction by Akt plus GHMT. Furthermore, addition of Akt1 to GHMT evoked a more mature cardiac phenotype for iCMs, as seen by enhanced polynucleation, cellular hypertrophy, gene expression, and metabolic reprogramming. Igf1 and Pi3 kinase acted upstream of Akt, whereas mTORC1 and Foxo3a acted downstream of Akt to influence fibroblast-to-cardiomyocyte reprogramming. These findings provide new insights into the molecular basis of cardiac reprogramming and represent an important step toward further application of this technique. Overall design: We performed RNA-Seq using either isolated adult mouse ventricular cardiomyocytes (CMs) or MEFs treated for three weeks with empty vector, GHMT (iCMs cell sorted using aMHC-GFP before RNA-Seq), or AGHMT (iCMs cell sorted using aMHC-GFP before RNA-Seq).

Publication Title

Akt1/protein kinase B enhances transcriptional reprogramming of fibroblasts to functional cardiomyocytes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE75126
L929 vs L929IRF8 following 4hr IFNbeta treatment (1000U/ml)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Identify genes like Ifit1 which are induced in L929 cells but not L929 cells expressing ectopic IRF8

Publication Title

Interferon Regulatory Factor 8 (IRF8) Impairs Induction of Interferon Induced with Tetratricopeptide Repeat Motif (IFIT) Gene Family Members.

Sample Metadata Fields

No sample metadata fields

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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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