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accession-icon GSE65576
Identification and molecular characterization of distinct glioblastoma cancer stem cell populations
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Malignant glioblastoma (GBM) is a highly aggressive brain tumor with a dismal prognosis and limited therapeutic options. Genomic profiling of GBM samples in the TCGA database has identified four molecular subtypes (Proneural, Neural, Classical and Mesenchymal), which may arise from different glioblastoma stem-like cell (GSC) populations. In the present study, we identify two GSC populations that produce GBM tumors by subcutaneous and intracranial injection with identical histological features. Gene expression analysis revealed that xenografts of GSCs grown as spheroid cultures had a Classical molecular subtype similar to that of bulk tumor cells. In contrast xenografts of GSCs grown as adherent cultures on laminin-coated plates expressed a Mesenchymal gene signature. Adherent GSC-derived xenografts had high STAT3 and ANGPTL4 expression as well as enrichment for stem cell markers, transcriptional networks and pro-angiogenic markers characteristic of the Mesenchymal subtype. Examination of clinical samples from GBM patients showed that STAT3 expression was directly correlated with ANGPTL4 expression, and that increased expression of these genes correlated with poor patient survival and performance. A pharmacological STAT3 inhibitor abrogated STAT3 binding to the ANGPTL4 promoter and exhibited anticancer activity in vivo. Taken together, we identified two distinct GSC populations that produce histologically identical tumors but with very different gene expression patterns, and a STAT3/ ANGPTL4 pathway in glioblastoma that may serve as a target for therapeutic intervention.

Publication Title

Molecular heterogeneity in a patient-derived glioblastoma xenoline is regulated by different cancer stem cell populations.

Alternate Accession IDs

E-GEOD-65576

Sample Metadata Fields

Specimen part

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accession-icon GSE61799
ICI182780 effect on breast cancer cell in hypoxia
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

The ER alpha positive breast cancer MCF7 cells were treated with ER alpha antagonist ICI182780 in normoxia and hypoxia. Extracted RNA was subject to microarray analysis. The goal of the experiment is to assess the ICI182780 effect on breast cancer cell in both normoxia and hypoxia.

Publication Title

Estrogen receptor-α directly regulates the hypoxia-inducible factor 1 pathway associated with antiestrogen response in breast cancer.

Alternate Accession IDs

E-GEOD-61799

Sample Metadata Fields

Cell line

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accession-icon GSE97209
R-spondin 2 is required for optic vesicle morphogenesis and neuroretina specification in vivo and in vitro
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Using stem cellbased therapies to treat retinal abnormalities is becoming a likely possibility; therefore, identifying the key factors and the relevant mechanisms controlling optic vesicle morphogenesis and neuroretina (NR) differentiation is important. Recent advances in self-organizing, 3-dimensional (3D) tissue cultures of embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) provided a valuable in vitro model for characterizing regulatory cascades and signaling pathways controlling mammalian retinal development. Using Rx-GFP expressing ESCs and Six3/ iPSCs we identified R-spondin 2 (Rspo2)-mediated repression of Wnt signaling as a novel required step during optic vesicle morphogenesis and NR differentiation. Furthermore, we also show that transient ectopic expression of Rspo2 in the anterior neural plate of transgenic mouse embryos was sufficient to arrest NR differentiation. ChIP assays identified Six3-responsive elements in the Rspo2-promoter region, indicating that Six3-mediated repression of Rspo2 is required to restrict Wnt signaling in the developing anterior neuroectoderm and allow eye development to proceed.

Publication Title

An Eye Organoid Approach Identifies Six3 Suppression of R-spondin 2 as a Critical Step in Mouse Neuroretina Differentiation.

Alternate Accession IDs

E-GEOD-97209

Sample Metadata Fields

Specimen part

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accession-icon GSE19069
Molecular signatures in peripheral T-cell lymphoma (PTCL)
  • organism-icon Homo sapiens
  • sample-icon 147 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Molecular signatures to improve diagnosis in PTCL and prognostication in angioimmunoblastic T-cell lymphoma (AITL). Gene expression profiling of PTCL patient samples was performed to investigate whether molecular signatures can be used to identify distinct entities of PTCL.

Publication Title

Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma.

Alternate Accession IDs

E-GEOD-19069

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP076990
Loss of Function Mutations in ETS2 Repressor Factor (ERF) Reveal a Balance Between Positive and Negative ETS Factors Controlling Prostate Oncogenesis [Organoids RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Half of prostate cancers are caused by a gene-fusion that enables androgens to drive expression of the normally silent ETS transcription factor ERG in luminal prostate cells1-4. Recent prostate cancer genomic landscape studies5-10 have reported rare but recurrent point mutations in the ETS repressor ERF11. Here we show these ERF mutations cause decreased protein stability and ERF mutant tumours are mostly exclusive from those with ERG fusions. ERF loss recapitulates the morphologic and phenotypic features of ERG gain in primary mouse prostate tissue, including expansion of the androgen receptor (AR) transcriptional repertoire, and ERF has tumour suppressor activity in the same genetic background of PTEN loss that yields oncogenic activity by ERG. Furthermore, in a human prostate cancer model of ERG gain and wild-type ERF, ChIP-seq studies indicate that ERG inhibits the ability of ERF to bind DNA at consensus ETS sites. Consistent with a competition model, ERF loss rescues ERG-positive prostate cancer cells from ERG dependency. Collectively, these data provide evidence that the oncogenicity of ERG is mediated, in part, by displacement of ERF and raise the larger question of whether other gain-of-function oncogenic transcription factors might also inactivate endogenous tumour suppressors. Overall design: Murine Pten+/+ prostates were infected with shNT or shErf lentivirus, selected with antibiotics and 2 rounds of FACS. For each condition, 2 sets of equal numbers of cells were plated and then processed for RNA extraction and RNA-seq independently.

Publication Title

ERF mutations reveal a balance of ETS factors controlling prostate oncogenesis.

Alternate Accession IDs

GSE83651

Sample Metadata Fields

Subject

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accession-icon GSE37165
Gene expression data from time course of fin regeneration in Danio rerio
  • organism-icon Danio rerio
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Alternate Accession IDs

E-GEOD-37165

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE37164
Gene expression data from time course of fin regeneration in Danio rerio (part 2)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Alternate Accession IDs

E-GEOD-37164

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE37163
Gene expression data from time course of fin regeneration in Danio rerio (part 1)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Alternate Accession IDs

E-GEOD-37163

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE90696
Identification of evolutionary conserved gene networks that mediate neurodegenerative dementia
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of evolutionarily conserved gene networks mediating neurodegenerative dementia.

Alternate Accession IDs

E-GEOD-90696

Sample Metadata Fields

Age, Specimen part, Time

View Samples
accession-icon SRP149532
Genome wide analysis of SAHA (vorinostat) treatment in human iPSC-derived neurons from Tau A152T patients and controls
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon

Description

Purpose: The goal of this study was to assess gene expression changes upon SAHA treatment in neurons derived from patients with A152T Tau mutation Overall design: iPSC derived neurons were treated with SAHA at different dosage for several days

Publication Title

Identification of evolutionarily conserved gene networks mediating neurodegenerative dementia.

Alternate Accession IDs

GSE115205

Sample Metadata Fields

No sample metadata fields

View Samples

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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