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accession-icon GSE39073
Expression data from a reversible dasatinib-resistant state in long-term dasatinib-treated c-KIT-mutated Kasumi-1 cell line
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Long-term treatment of Kasumi-1 cells at clinically attained doses of dasatinib led to decreased drug-sensitivity by means of IC50 values (relative to treatment-naive cells). Changes were paralled by profound alterations in c-KIT expression and cell signaling signatures. Upon brief discontinuation of dasatinib treatment, these alterations reversed and drug sensitivity was restored.

Publication Title

Transitory dasatinib-resistant states in KIT(mut) t(8;21) acute myeloid leukemia cells correlate with altered KIT expression.

Sample Metadata Fields

Cell line

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accession-icon GSE37934
Differential gene expression profiles between SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid).
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To dissect the molecular mechanisms of PEA-15-mediated paclitaxel sensitization in ovarian cancer cells, we performed cDNA microarray analysis using SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid). cDNA microarray data analysis showed that SCLIP (SCG10-like protein), also known as STMN3, was highly expressed in SKOV3.ip1-S116D cells and was involved in pPEA-15-mediated paclitaxel sensitization in ovarian cancer cells.

Publication Title

Bisphosphorylated PEA-15 sensitizes ovarian cancer cells to paclitaxel by impairing the microtubule-destabilizing effect of SCLIP.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE31409
Lentiviral vector-based insertional mutagenesis identifies new clinically relevant cancer genes involved in the pathogenesis of hepatocellular carcinoma
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We devised a novel insertional mutagenesis approach based on lentiviral vectors to induce hepatocellular carcinoma in three mouse models and identified four novel cancer initiating genes. Two genes are the well characterized Braf and Sos1, while the other two are Fign, encoding an AAA ATPase whose functions are poorly understood, and the complex Dlk1-Dio3 imprinted region which has been recently implicated in cancer and stemness. Activation of Fign or Braf and upregulation of the Dlk1-Dio3 imprinted region are functionally interconnected and may altogether control cell transformation, stemness and energy metabolism. Moreover, all the genes identified play a relevant role in human hepatocarcinogenesis as their expression levels and/or transcriptional signatures induced by their deregulation predict a different clinical outcome in hepatocellular carcinoma patients. These series consists of mRNA expression microarray data (The GeneChip Mouse Gene 1.0 ST Array, Affymetrix) from 8 non-tumoral liver and 21 hepatocellular carcinoma induced by insertional mutagenesis.

Publication Title

Lentiviral vector-based insertional mutagenesis identifies genes associated with liver cancer.

Sample Metadata Fields

Specimen part

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accession-icon SRP081252
Loss of Snf5 and the formation of an aberrant SWI/SNF complex
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Aberrant forms of the SWI/SNF chromatin remodeling complex are associated with human disease. Loss of the Snf5 subunit of SWI/SNF is a driver mutation in pediatric rhabdoid cancers and forms aberrant sub-complexes that are not well characterized. We determined the effects of loss of Snf5 on the composition, nucleosome binding, recruitment and remodeling activities of yeast SWI/SNF. The Snf5 subunit interacts with the ATPase domain of Snf2 and forms a submodule consisting of Snf5, Swp82 and Taf14 as shown by mapping SWI/SNF subunit interactions by crosslinking-mass spectrometry and subunit deletion followed by immunoaffinity chromatography. Snf5 promoted binding of the Snf2 ATPase domain to nucleosomal DNA, enhanced its catalytic activity and facilitated nucleosome remodeling. Snf5 was required for acidic transcription factors to recruit SWI/SNF to chromatin. RNA-seq analysis suggested that both the recruitment and catalytic functions mediated by Snf5 are required for SWI/SNF regulation of gene expression. Overall design: Determining the effects of loss of Snf5 on the composition, nucleosome binding, recruitment, remodeling activities and gene expression profile of yeast SWI/SNF

Publication Title

Loss of Snf5 Induces Formation of an Aberrant SWI/SNF Complex.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE23293
Definition and characterization of the systemic T cell dysregulation in untreated indolent B cell lymphoma and very early CLL
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Epidemiological data show that the immune system may control or promote emergence and growth of a neoplastic lymphomatous clone. Conversely, systemic lymphomas, especially myeloma and CLL, are associated with clinical immunodeficiency. This prospective controlled study demonstrates substantially reduced circulating T helper cells, predominantly naive CD4+ cells, in patients with non-leukemic follicular and extranodal marginal zone lymphomas, but not in monoclonal gammopathy and early CLL. These numerical changes were correlated with a preactivated phenotype, hyperreactivity in vitro, presenescence, and a Th2 shift of peripheral T helper cells. No prominent alterations were found in the regulatory T cell compartment. Gene expression profiling of in vitro-stimulated CD4+ cells revealed an independent second alteration of T helper cell physiology which was most pronounced in early CLL but also detectable in FL/eMZL. This pattern consisted of downregulation of proximal and intermediate T-cell receptor signaling cascades and globally reduced cytokine secretion. Both types of T cell dysfunction may contribute to significant immunodeficiency in non-leukemic indolent B-cell lymphomas as demonstrated by refractoriness to hepatitis B vaccination. The precise definition of systemic T cell dysfunction serves as the basis to study its prognostic impact, its relationship to the established influence of the lymphoma microenvironment, and its therapeutic manipulation

Publication Title

Definition and characterization of the systemic T-cell dysregulation in untreated indolent B-cell lymphoma and very early CLL.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE24225
Expression analysis of mouse embryo fibrobalsts lacking Tgif1
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Tgif1 is a transcriptional corepressor that limits TGF responsive gene expression. TGF signaling has antiproliferative effects in several cell types, generally resulting in a G1 arrest. Mouse embryo fibroblasts (MEFs) are primary cells with limited life-span, that senesce after several passages in culture.

Publication Title

Premature senescence and increased TGFβ signaling in the absence of Tgif1.

Sample Metadata Fields

Specimen part

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accession-icon GSE37580
Identification of differentially expressed genes upon treatment with Eltrombopag in HL60 cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Identification of differentially expressed genes upon treatment with Eltrombopag in HL60 cells. HL60 cells were untreated, or treated with 3ug/ml of Eltrombopag for 36 hrs in RPMI with 10% FBS

Publication Title

Eltrombopag inhibits the proliferation of leukemia cells via reduction of intracellular iron and induction of differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE7755
Gene expression in fetal gubernaculum and testis of wildtype (LE/wt) and cryptorchid (LE/orl) rats
  • organism-icon Rattus norvegicus
  • sample-icon 54 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

The Long Evans/orl (LE/orl) rat is an animal model of inherited undescended testis (UDT). To explore genetic mechanisms of UDT, we studied differential gene expression in LE/orl and LE wild type (LE/wt) fetal gubernaculum and testis.

Publication Title

Altered expression of muscle- and cytoskeleton-related genes in a rat strain with inherited cryptorchidism.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE19658
Gene Profiling Male Fetal Rat Gubernaculum After Insulin-like 3 (Insl3) Exposure
  • organism-icon Rattus norvegicus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Insl3 is a testis-derived hormone that induces growth and differentiation of the fetal gubernaculum. The goal of this study was to identify genes showing altered expression in fetal gubernaculum following Insl3 exposure.

Publication Title

Insulin-like 3 exposure of the fetal rat gubernaculum modulates expression of genes involved in neural pathways.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE144901
CLL intraclonal fractions exhibit established and recently-acquired patterns of DNA methylation
  • organism-icon Homo sapiens
  • sample-icon 103 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

CLL intraclonal fractions exhibit established and recently acquired patterns of DNA methylation.

Sample Metadata Fields

Sex, Specimen part, Subject

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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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