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accession-icon GSE59874
PIK3CA(H1047R)-evoked breast tumorigenesis
  • organism-icon Mus musculus
  • sample-icon 49 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

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE40875
Early parity-induced gene expression in mouse mammary cell subtypes
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the effect of early pregnancy on the gene expression profiles of stromal and various epithelial mammary cell subpopulations in mice.

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE59872
Gene expression profiling of Lgr5-creERT2/PIK3CA H1047R and K8-creERT2/PIK3CA H1047R-evoked mammary tumors
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the gene expression profile of mammary tumors derived from Lgr5- and K8-positive cell-of-origins

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE59870
Gene expression profiling of preneoplastic Lgr5-creERT2/PIK3CAH1047R mammary subsets
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from Lgr5-creERT2/PIK3CA H1047R mice

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE65411
Gene expression profiling of preneoplastic K8-creERT2/PIK3CAH1047R mammary subsets
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from K8-creERT2/PIK3CA H1047R mice

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Treatment, Time

View Samples
accession-icon GSE46797
Expression data from c-Myc+ Notch1 T-ALL initiating cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Missense FBXW7 mutations are prevalent in various tumors, including T-cell acute lymphoblastic leukemia (T-ALL). To study the effects of such lesions, we generated animals carrying regulatable Fbxw7 mutant alleles. We show here that these mutations specifically bolster cancer-initiating cell activity in collaboration with Notch1 oncogenes, but spare normal hematopoietic stem cell function. We were also able to show that FBXW7 mutations specifically affect the ubiquitylation and half-life of c-Myc protein, a key T-ALL oncogene. Using animals carrying c-Myc fusion alleles, we connected Fbxw7 function to c-Myc abundance and correlated c-Myc expression to leukemia-initiating activity.

Publication Title

The ubiquitin ligase FBXW7 modulates leukemia-initiating cell activity by regulating MYC stability.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE27816
Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation.

Publication Title

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP072417
NextGen Consortium: GENESiPS Study: Identifying the Gene Networks of Insulin Resistance
  • organism-icon Homo sapiens
  • sample-icon 317 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNA-seq transcriptome profiling of human induced pluripotent stem cells to characterize gene expression variation across individuals and within multiple iPSC lines from the same individual Overall design: Donor erythroblast or activated T-cells were reprogrammed with a Sendai viral vector coding for reprogramming factors. IPSC lines were propagated for ~9 passages before RNA sequencing

Publication Title

Analysis of Transcriptional Variability in a Large Human iPSC Library Reveals Genetic and Non-genetic Determinants of Heterogeneity.

Sample Metadata Fields

Sex, Age, Race, Subject

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accession-icon SRP076097
TLR2/1 ligand and IFN-g inducible genes in human monocyte-derived macrophages (MDMs)
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptome profiles for innate and adaptive immune stimuli important for host response against mycobacteria. Human monocyte-derived macrophages were stimulated with TLR2/1 ligand and interferon-g, stimuli present during innate and adaptive immune responses, respectively. Overall design: Human monocyte-dervided macrophages from five healthy donors were stimulated with TLR2/1L, IFN-g, or media control for 2, 6, and 24 hours. RNA-sequencing was performed on a total of 45 samples.

Publication Title

S100A12 Is Part of the Antimicrobial Network against Mycobacterium leprae in Human Macrophages.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE12831
The role of qseE, qseF and qseG in the regulation of EHEC virulence
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Escherichia coli 8624 and the isogenic mutants in qseE, qseF and qseG are compared to determine the role that each of the genes play in regulation of the transcriptome. These results are verified by qRT-PCR and reveal the important role of this three-component signaling system.

Publication Title

The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis.

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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