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accession-icon E-MEXP-369
Transcription profiling of mouse non-transformed cell (NIH3T3 + vector) and a transformed cell (NIH3T3 + Fbxo7)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The aim of this experiment was to get a comparison of the signatures between a non-transformed cell (NIH3T3 + vector) and a transformed cell (NIH3T3 + Fbxo7). NIH3T3 cells become transformed after the stable integration of the Fbxo7 gene. Fbxo7 potentiates cyclin D/cdk6 activity.

Publication Title

Transforming activity of Fbxo7 is mediated specifically through regulation of cyclin D/cdk6.

Sample Metadata Fields

Cell line

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accession-icon E-MEXP-466
Transcription profiling of two populations of non-hematopoetic stem cells (MSC and MAPC) isolated from human bone marrow
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Compare the behaviour of two populations of non-hematopoetic stem cells (MSC and MAPC) isolated from human bone marrow. The effect of culture conditions on the behaviour of MSC was also characterised by isolating MSC and then culturing the cells for 96h in MAPC growth conditions

Publication Title

Validation of COL11A1/procollagen 11A1 expression in TGF-β1-activated immortalised human mesenchymal cells and in stromal cells of human colon adenocarcinoma.

Sample Metadata Fields

Age, Specimen part

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accession-icon E-MEXP-66
Transcription profiling of Kaposi sarcoma, normal skin and primary cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Identification of the relationships of Kaposi sarcoma (KS), normal skin to various cell cultures. The effects of KS herpes virus, the infectious cause of KS, on infected endothelial cells are also investigated.

Publication Title

ARID3B induces malignant transformation of mouse embryonic fibroblasts and is strongly associated with malignant neuroblastoma.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Cell line, Subject

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accession-icon SRP153919
Hyperactivation of MAPK signaling is deleterious to RAS/RAF mutant melanoma
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The most frequent genetic alterations in melanoma are gain-of-function mutations in BRAF, which result in addiction to the RAF-MEK-ERK signaling pathway. Despite success of RAF and MEK inhibitors in treating BRAFV600 mutant tumors, a major challenge is the inevitable emergence of drug resistance, which often involves reactivation of the MAPK pathway. Interestingly, resistant tumors are often sensitive to drug withdrawal, suggesting that hyperactivation of the MAPK pathway is not tolerated. To further characterize this phenomenon, we generated isogenic models of inducible MAPK hyperactivation in BRAFV600E melanoma cells by overexpression of ERK2. Using this model system, we demonstrated that supra-physiological levels of MAPK signaling led to cell death, which was reversed by MAPK inhibitors. Whereas MAPK pathway inhibition led to cell stasis in BRAFV600E melanoma cells, MAPK hyperactivation induced cytotoxicity. Furthermore, complete tumor regression was observed in an ERK2 overexpressing xenograft model. To identify mediators of MAPK hyperactivation- induced cell death, we conducted a large-scale pooled screen which showed that only shRNAs against BRAF and MAP2K1 rescued loss of cell viability. This suggested that no single downstream ERK2 effector was required, consistent with pleiotropic effects on multiple cellular stress pathways. Intriguingly, the detrimental effect of MAPK hyperactivation could be partially attributed to secreted factors, and more than 100 differentially secreted proteins were identified. The effect of ERK2 overexpression was highly context dependent, as RAS/RAF mutant but not RAS/RAF wildtype melanoma were sensitive to this perturbation. This vulnerability to MAPK hyperactivation raises the possibility of a novel therapeutic approach for RAS/RAF mutant cancers.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease, Cell line, Treatment

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accession-icon E-MEXP-122
Transcription profiling of leukemic cells of monozygotic twins
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We established gene expression profiles of diagnostic bone marrow samples of monozygotic twins with acute lymphoblastic leukemia. We established technical duplicates for each twin.

Publication Title

Prenatal origin of separate evolution of leukemia in identical twins.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon SRP068424
Homo sapiens Raw sequence reads
  • organism-icon Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Type-1 interferons are critical for inhibiting HIV and simian immunodeficiency virus. However, it is largely unknown which of the hundreds of interferon-stimulated genes (ISGs) restrict HIV replication (with the notable exceptions of APOBEC3G, MX2, and BST-2). To identify HIV restriction factors, we sequenced activated CD4+ T cell RNA from 19 humans with untreated HIV infection before and after peginterferon alpha 2b (IFN) injection. Antiretroviral therapy (ART) durably suppresses HIV-1, prevents progression to acquired immunodeficiency syndrome, and reduces mortality. However, even with ART HIV-1 infected adults remain at higher risk of death from inflammatory disease. To understand the role of ART in altering cell-associated HIV RNA and host RNA changes within activated CD4 T cells we also sequenced activated CD4 T cell RNA from these same 19 humans after initiating ART and obtaining =12 weeks of undetectable viremia.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP068551
Transcriptome sequencing identified hub genes for hepatocellular carcinoma by weighted-gene co-expression analysis
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

To conduct clinical cancer research and study the genetic basis of hepatocellular carcinoma

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP103099
Patient derived xenograft models of leukemia and lymphoma whole transcriptome sequencing
  • organism-icon Homo sapiens
  • sample-icon 121 Downloadable Samples
  • Technology Badge Icon

Description

To facilitate preclinical translational science, this cohort of patient-derived xenograft (PDX) models of leukemia and lymphoma has undergone molecular characterization with whole transcriptome sequencing, targeted exon sequencing of genes recurrently altered in leukemia and lymphoma, and other approaches. Here we provide the whole transcriptome sequencing data for these PDX models. Related molecular data and de-identified clinical information can be obtained at http://www.proxe.org.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE68162
Expression data from MAP3K11/GDF15 axis is a critical driver of cancer cachexia
  • organism-icon Mus musculus
  • sample-icon 76 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

MAP3K11 overexpression in tumors leads to weight loss in the host

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE59808
Expression data from AML cell lines
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Post-chemotherapy relapse presents a major unmet medical need in AML where treatment options are limited. We used gene expression profile from 32 AML cell lines to characterize expression difference between responder and non-responders to PIM inhibitors. Our results highlight the importance of STAT5 and MYC in rendering cancer cells sensitive to PIM inhibitors.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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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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Developed by the Childhood Cancer Data Lab

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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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