refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 156 results
Sort by

Filters

Technology

Platform

accession-icon GSE26298
Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor 1 apoprotein
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor 1 apoprotein.

Publication Title

During hormone depletion or tamoxifen treatment of breast cancer cells the estrogen receptor apoprotein supports cell cycling through the retinoic acid receptor α1 apoprotein.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP171067
Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Plexiform neurofibroma is a major contributor to morbidity in Neurofibromatosis type I (NF1) patients. Macrophages and mast cells infiltrate neurofibroma, and data from mouse models implicate these leukocytes in neurofibroma development. Anti-inflammatory therapy targeting these cell populations has been suggested as a means to prevent neurofibroma development. Here, we compare gene expression in inflamed nerves from NF1 models which invariably form neurofibroma to those with inflammation driven by EGFR overexpression which rarely progresses to neurofibroma. We find that the chemokine Cxcl10 is uniquely up-regulated in NF1 mice that invariably develop neurofibroma. Global deletion of the CXCL10 receptor, Cxcr3, prevented neurofibroma development in these neurofibroma-prone mice. Cxcr3 expression localized to T cells and dendritic cells (DCs) in both inflamed nerves and neurofibromas. These data support a heretofore unappreciated role for T cells/DCs in neurofibroma initiation. Overall design: To identify cell populations associated with Cxcl10 expression, we utilized a single-cell RNA-Seq (scRNA-Seq) data set collected from 2-month Dhh-Cre;Nf1 fl/fl nerve/DRG using the 10x Genomics Chromium platform.

Publication Title

Cxcr3-expressing leukocytes are necessary for neurofibroma formation in mice.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

View Samples
accession-icon GSE59545
NF-kB in Tumor Initiation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

p65-/-Ras cells show delayed tumor formation in SCID mice. However, after prolonged latency, tumor formation was observed from these mice. To understand the changes of NF-kB regulated genes before and after tumor formation, RNA from p65+/+Ras, p65+/+RasTumor, p65-/-Ras, p65-/-RasTumor cells were isolated and microarray were performed.

Publication Title

NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP114773
Transcriptome-wide analysis of the role of HTLV-1 Tax PBM in T-Cells from infected humanized-mice (hu-Mice)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Human T-lymphotropic virus type 1 (HTLV-1) is associated with the development of Adult T-cell Leukemia, an aggressive CD4+ T-cells malignancy. Here, we have developed a new procedure to infect humanized mice with proviruses displaying specific mutations, such as one leading to the loss of the PDZ domain-binding motif (PBM) of Tax. In order to specifically analyze the in vivo role of the PBM of Tax, a comparative study of infected hu-mice was performed. We used next-generation sequencing to perform genome-wide transcriptomic analysis of T-cells infected with wild-type HTLV-1 virus or with virus bearing a mutated form of Tax lacking the PBM. Our results suggest that Tax PBM might be involved in the regulation of genes implicated in proliferation, apoptosis and cytoskeleton organization. Overall design: mRNA profiles of T-cells obtained from hu-Mice infected with wild-type or Tax-PBM HTLV-1 were generated by deep-sequencing in triplicates using Illumina's Hiseq3000 platform.

Publication Title

PDZ domain-binding motif of Tax sustains T-cell proliferation in HTLV-1-infected humanized mice.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE34589
Elk1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Elk1 directs selective gene induction that is a substantial and critical component of growth signaling by AR in PC cells.

Publication Title

The ETS domain transcription factor ELK1 directs a critical component of growth signaling by the androgen receptor in prostate cancer cells.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE41747
MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors, despite transcriptional feedback onto ERK.
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 83 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Neurofibromatosis Type 1 (NF1) patients develop benign neurofibromas and malignant peripheral nerve sheath tumors (MPNST). These incurable peripheral nerve tumors result from loss of NF1 tumor suppressor gene function, causing hyperactive Ras signaling. Activated Ras controls numerous downstream effectors, but specific pathways mediating effects of hyperactive Ras in NF1 tumors are unknown. Cross-species transcriptome analyses of mouse and human neurofibromas and MPNSTs identified global negative feedback of genes that regulate Ras-Raf- MEK- extracellular signal-regulated protein kinase (ERK) signaling in both species. Nonetheless, activation of ERK was sustained in mouse and human neurofibromas and MPNST. PD0325901, a highly selective pharmacological inhibitor of MEK, was used to test whether sustained Ras-Raf-MEK-ERK signaling contributes to neurofibroma growth in the Nf1fl/fl;Dhh-cre mouse model or in NF1 patient MPNST cell xenografts. PD0325901 treatment reduced aberrantly proliferating cells in neurofibroma and MPNST, prolonged survival of mice implanted with human MPNST cells, and shrank neurofibromas in >80% of mice tested. PD0325901 also caused effects on tumor vasculature. Our data demonstrate that deregulated Ras/ERK signaling is critical for the growth of NF1 peripheral nerve tumors and provide strong rationale for testing MEK inhibitors in NF1 clinical trials.

Publication Title

MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE22483
Hormone-Independence of Prostate Cancer Cells is Supported by the Androgen Receptor without Binding to Classical Response Elements
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Treatment of late passage (LP50) LNCaP cells with R1881 (androgen) and AR shRNA identified a gene program controlled by androgen receptor in the absence of androgen.

Publication Title

Hormone depletion-insensitivity of prostate cancer cells is supported by the AR without binding to classical response elements.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE14038
Integrative genomic analyses of neurofibromatosis tumors identify SOX9 as biomarker and survival gene
  • organism-icon Homo sapiens
  • sample-icon 85 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Understanding biological pathways critical for common neurofibromatosis type 1 (NF1) peripheral nerve tumors is essential, as tumor biomarkers, prognostic factors and therapeutics are all lacking. We used gene expression profiling to define transcriptional changes between primary normal Schwann cells (n = 10), NF1-derived primary benign neurofibroma Schwann cells (n = 22), malignant peripheral nerve sheath tumor (MPNST) cell lines (n = 13), benign neurofibromas (n = 26) and MPNST (n = 6). Dermal and plexiform neurofibromas were indistinguishable. A prominent theme in the analysis was aberrant differentiation. Neurofibromas repressed gene programs normally active in Schwann cell precursors and immature Schwann cells. MPNST signatures strongly differed; genes upregulated in the sarcomas were significantly enriched for genes activated in neural crest cells. We validated differential expression of 82 genes including the neural crest transcription factor SOX9 and SOX9 predicted targets. SOX9 immunoreactivity was robust in neurofibroma and MPSNT tissue sections and targeting SOX9 - strongly expressed in NF1-related tumors - caused MPNST cell death. SOX9 is a biomarker of neurofibroma and MPNST, and possibly a therapeutic target in NF1.

Publication Title

Integrative genomic analyses of neurofibromatosis tumours identify SOX9 as a biomarker and survival gene.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP076036
Next Generation Sequencing Facilitates Quantitative Analysis of human patient derived primary Glioblastoma (GBM) cancer cell Transcriptomes
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare GBM transcriptome profiling (RNA-seq) after shRNA based knockdown of PRKAB1 and to compare gene expression by optimal high-throughput data analysis Overall design: Methods: Total RNA profiles of two GBM cells (scramble and PRKAB1 sh RNA treated) were generated by deep sequencing, in triplicate, using Illumina Hiseq 2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using SYBR Green assays

Publication Title

AMP kinase promotes glioblastoma bioenergetics and tumour growth.

Sample Metadata Fields

Specimen part, Race, Subject

View Samples
accession-icon E-MEXP-2818
Transcription profiling by array of yeast desiccation stress response in a time series
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Response of Saccharomyces cerevisiae strain BY4741 to desiccation

Publication Title

Phenomic and transcriptomic analyses reveal that autophagy plays a major role in desiccation tolerance in Saccharomyces cerevisiae.

Sample Metadata Fields

Time

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact