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accession-icon GSE55983
Inflammation-induced chemokine expression in uveal melanoma cell lines stimulates monocyte chemotaxis
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Purpose: Uveal melanoma (UM) is the most common primary intraocular tumor in adults and the presence of infiltrating leucocytes is associated with a poor prognosis. Little is known how infiltrating leucocytes influence the tumor cells. The purpose of this study was to investigate the effect of activated T cells on the expression of chemotactic cytokines in UM cells. Furthermore, we examined the ability of stimulated UM cells to attract monocytes.

Publication Title

Inflammation-induced chemokine expression in uveal melanoma cell lines stimulates monocyte chemotaxis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP040306
Transcriptome of wild-type and G9a mutant upon viral challenge
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The aim of the study was to generate transcriptome of wild-type and G9a mutant adult flies (females) 24h post-infection with Drosophila C Virus (DCV). Overall design: We generated 8 different data sets. For wild-type controls and G9a mutants, we performed both mock and DCV infection, and collected both whole flies and fat bodies. All flies were 3-5 days old females.

Publication Title

The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon SRP071848
Tdrd6a recruits Ziwi-bound piRNAs and coordinates deposition of germ plasm mRNAs into primordial germ cells [scRNA-Seq]
  • organism-icon Danio rerio
  • sample-icon 100 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Germ plasm, the Balbiani body and nuage are evolutionary conserved structures essential for germ cell specification and maintenance. We describe Tdrd6a as a component of these structures with two distinct molecular functions. First, Tdrd6a facilitates the accumulation of the typical antisense-bias of piRNAs, without having effects on piRNA biogenesis signatures. Second, we show that Tdrd6a is required for Balbiani body and germ plasm integrity, and associates with RNA-binding proteins and germ plasm mRNAs. On the cell-biological level, maternally contributed Tdrd6a strongly impacts germ cell formation, but is dispensable for fertility. Using single-cell RNA-sequencing we demonstrate that Tdrd6a promotes early germ cell development and regulates the stoichiometry of germ plasm mRNAs. We propose that Tdrd6a functions as a scaffold to recruit correct ratios of germ plasm transcripts and to accumulate antisense piRNA complexes in order to ensure both specification and maintenance of germ cells. Overall design: Single cell were sorted directly in Trizolfrom embryos spawned by mz tdrd6a-/- mother and wt mother carrying a kop::egfp-f-nos1-3'UTR transgene. Thereafter single cell trizol extractio was performed followed by RT, IVT and RNA-seq library prep.

Publication Title

Tdrd6a Regulates the Aggregation of Buc into Functional Subcellular Compartments that Drive Germ Cell Specification.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE18592
Estrogen Coordinates Translation and Transcription Revealing a Role for NRSF in Human Breast Cancer Cells
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Analysis of estrogen receptor (ER)-positive MCF7 cell total RNA expression and polysome-assiciated RNA expression following treatment with estradiol (E2) and vehicle (etoh).

Publication Title

Estrogen coordinates translation and transcription, revealing a role for NRSF in human breast cancer cells.

Sample Metadata Fields

Cell line

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accession-icon GSE77498
Induced loss of p53 in mammary luminal cells leads to their clonal expansion and facilitates development of mammary tumours with loss of luminal identity
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Diversity Genotyping Array (mousedivm520650), Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Induced p53 loss in mouse luminal cells causes clonal expansion and development of mammary tumours.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE14753
Mammary tumors from K14-cre; ApcCKO/+ mice vs control mammary glands
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Many components of Wnt/-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of -catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of -catenin signaling optimal for mammary tumor development.

Publication Title

Genetic mechanisms in Apc-mediated mammary tumorigenesis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE114438
A PDGFR-driven mouse model of Glioblastoma reveals a Stathmin1-mediated mechanism of sensitivity to Vinblastine
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Glioblastoma multiforme (GBM) is an aggressive primary brain cancer that includes focal amplification of PDGFR and for which there are no effective therapies. Herein, we report the development of a genetically engineered mouse model of GBM based on autocrine, chronic stimulation of PDGFR and the analysis of GBM signaling pathways using proteomics. We discovered the tubulin-binding protein Stathmin1 (STMN1) as a PDGFR phospho-regulated target and that this mis-regulation conferred selective sensitivity to vinblastine (VB) cytotoxicity. Treatment of PDGFR GBMs with VB in mice drastically prolonged survival and was dependent on STMN1. Our work provides a rationale for evaluating genotype-specific anti-microtubule drugs as cancer treatment in select GBM patient populations.

Publication Title

A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE61758
Effect of loss of PKC theta and p50+cRel on gene expression post T-cell stimulation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

OT-1 Transgenic CD8 T-cells were isolated from spleens of WT, PKC theta KO, and p50 cRel DKO mice. The T-cells were either cultured with non-pulsed DC (WT only and signified as "WT - UN") or with BMDCs pulsed with the OVA peptide SIINFEKL (N4) (WT, PKC theta KO, and p50 cRel DKO and signified as 'genotype - N4') at a ratio of 1:10 (DC:T-cell) for 18 hours. DCs then were depleted from the culture and RNA was made from the T-cells to measure gene expression at the early / late stage of T-cell activation

Publication Title

NF-κB is crucial in proximal T-cell signaling for calcium influx and NFAT activation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE92473
Microarray expression profiling data for sorted prostate epithelial subpopulations based on LY6D
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

In the normal prostate, most basal and some luminal cells are castration-resistant (CR). The identity of these CR cells and their relation to CR prostate cancer are unresolved. We compared single-cell expression profiles of prostate cells sorted from hormonally nave (HN) and castrated mice. We found both basal and luminal-localized cells, particularly the latter, were molecularly heterogeneous. CR luminal cells and a subset of HN luminal cells exhibited a similar intermediate expression pattern, including high-level expression of multiple prostate stem/progenitor marker genes and androgen receptor gene. We validated LY6D as a marker linking CR luminal cells to luminal progenitors. LY6D+ prostate cells, including LY6D+ luminal cells, were enriched for organoid-forming potential regardless of the presence or absence of androgen. Krt8-based lineage-tracing revealed that LY6D+ CR luminal cells produced LY6D- normal luminal cells upon regeneration, but LY6D+ luminal cancer cells under PTEN-deficiency. Furthermore, prostate cancers originating from CR luminal cells (LY6D+) exhibited a more advanced phenotype than those from HN luminal cells (LY6D+ or LY6D-). Lastly, LY6D amplification/upregulation appear associated with advanced prostate cancer in patient samples. Together, our studies demonstrate LY6D as a novel progenitor marker predictive of lethal CR disease.

Publication Title

Single-Cell Analysis Identifies LY6D as a Marker Linking Castration-Resistant Prostate Luminal Cells to Prostate Progenitors and Cancer.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE7035
Synergy between PPARgamma ligands and platinum-based drugs in cancer
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

PPAR is a member of the nuclear receptor family for which agonist ligands have anti-growth effects. However, clinical studies using PPAR ligands as a monotherapy failed to show a beneficial effect. Here we have studied the effects of PPAR activation with chemotherapeutic agents in current use for specific cancers. We observed a striking synergy between rosiglitazone and platinum-based drugs in several different cancers both in vitro and using transplantable and chemically induced spontaneous tumor models. The effect appears to be due in part to PPAR-mediated downregulation of metallothioneins, proteins that have been shown to be involved in resistance to platinum-based therapy. These data strongly suggest combining PPAR agonists and platinum-based drugs for the treatment of certain human cancers

Publication Title

Synergy between PPARgamma ligands and platinum-based drugs in cancer.

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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