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accession-icon GSE58771
Expression data from Arabidopsis thaliana root and piriformaspora indica during log and short term interaction
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Piriformospora indica, an endophytic fungus of Sebacinales, colonizes the roots of many plant species including Arabidopsis thaliana. The symbiotic interaction promotes plant per-formance, growth and resistance/tolerance against abiotic and biotic stress. We demonstrate that exudated compounds from the fungus activate stress and defense responses in the Arabidopsis roots and shoots before the two partners are in physical contact. They induce stomata closure, stimulate reactive oxygen species (ROS) production, stress-related phytohormone accumulation and activate defense and stress genes in the roots and/or shoots. Once a physical contact is established, the stomata re-open, ROS and phytohormone levels decline, and the gene expression pattern indicates a shift from defense to mutualistic interaction.

Publication Title

The interaction of Arabidopsis with Piriformospora indica shifts from initial transient stress induced by fungus-released chemical mediators to a mutualistic interaction after physical contact of the two symbionts.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP200955
Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wildtype ESR1. The D538G mutation impacted expression, including a large set of non-estrogen regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is unique from constitutive ESR1 activity as mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells. Overall design: RNA-seq was used to study the effects of the D538G mutation on gene expression

Publication Title

Estrogen-independent molecular actions of mutant estrogen receptor 1 in endometrial cancer.

Sample Metadata Fields

Cell line, Treatment, Subject, Time

View Samples
accession-icon GSE6351
Expression data from peripheral blood from healthy and predisposed individuals
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Characterization of the underlying genetic defects in patients with a rare and peculiar phenotype is challenging. Here we have utilized whole genome expression profiling, and identified a homozygous germline mutation in the DDB2 gene in a patient with several facial tumors. The feasibility of using blood derived RNA, diminishing costs of the technology, and the limited number of samples needed provide this approach a powerful new tool that may substantially aid in such gene identification efforts.

Publication Title

Blood-derived gene-expression profiling in unravelling susceptibility to recessive disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP131796
Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor a in endometrial cancer [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Steroid hormone receptors are simultaneously active in many tissues and capable of altering each other's function. Estrogen receptor ? (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors expressing high levels of ER, we surprisingly found that expression of GR is associated with poor prognosis. Dexamethasone reduced normal uterine growth in vivo; however, this growth inhibition was abolished in estrogen-induced endometrial hyperplasia. We observed low genomic binding site overlap when ER and GR are induced with their respective ligands; however, upon simultaneous induction they co-occupy more sites. GR binding is significantly altered by estradiol with GR recruited to ER bound loci that become more accessible upon estradiol induction. Gene expression responses to co-treatment were more similar to estradiol, but with novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer. Overall design: ChIP-seq, ATAC-seq, and RNA-seq data collected from endometrial cancer cell lines induced with dexamethasone, estradiol, or the combination

Publication Title

FFPEcap-seq: a method for sequencing capped RNAs in formalin-fixed paraffin-embedded samples.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE47109
BreastPRS is a Gene Expression Assay that Stratifies Intermediate-Risk Oncotype DX Patients into High or Low-Risk for Disease Recurrence
  • organism-icon Homo sapiens
  • sample-icon 239 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Molecular prognostic assays, such as Oncotype DX, are increasingly incorporated into the management of patients with invasive breast carcinoma. BreastPRS is a new molecular assay developed and validated from a meta-analysis of publically available genomic datasets. We applied the assay to matched fresh-frozen (FF) and formalin-fixed paraffin embedded (FFPE) tumor samples to translate the assay to FFPE. A linear relationship of the BreastPRS prognostic score was observed between tissue preservation formats. BreastPRS recurrence scores were compared with Oncotype DX recurrence scores from 246 patients with invasive breast carcinoma and known Oncotype DX results. Using this series, a 120-gene linear discriminant algorithm (LDA) was trained to predict Oncotype DX risk groups and then applied to series of untreated, node-negative, estrogen receptor (ER) positive patients from previously published studies with known clinical outcomes. Correlation of recurrence score and risk group between Oncotype DX and BreastPRS was statistically significant (P<0.0001). 59 of 260 (23%) patients from four previously published studies were classified as intermediate-risk when the 120-gene LDA was applied. BreastPRS reclassified the 59 patients into binary risk groups (high vs. low-risk). 23 (39%) patients were classified as low-risk 36 (61%) as high-risk [P=0.029, HR: 3.64, 95% CI: 1.40 to 9.50]. At 10 years from diagnosis, the low-risk group had a 90% recurrence-free survival (RFS) rate, compared to 60% for the high-risk group. BreastPRS recurrence score is comparable to Oncotype DX and can reclassify Oncotype DX intermediate-risk patients into two groups with significant differences in RFS. Further studies are needed to validate these findings.

Publication Title

BreastPRS is a gene expression assay that stratifies intermediate-risk Oncotype DX patients into high- or low-risk for disease recurrence.

Sample Metadata Fields

Disease stage

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accession-icon GSE24450
183 breast tumors from the Helsinki Univerisity Central Hospital with survival information
  • organism-icon Homo sapiens
  • sample-icon 183 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

183 breast tumors from the Helsinki Univerisity Central Hospital with survival information

Publication Title

Variants on the promoter region of PTEN affect breast cancer progression and patient survival.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18323
Expression data from a malaria vaccine trial (HG-U133A2.0 and U133 Plus 2.0)
  • organism-icon Homo sapiens
  • sample-icon 254 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Volunteers were assessed at study entry, the day of the third vaccination and 24, 72 hours, two weeks after vaccination, and 5 days after challenge. 13/39 vaccinees were protected and 26/39 were not protected. Eleven vaccinees exhibited delayed onset of parasitemia. All infectivity controls developed parasitemia. Prediction Analysis of Microarrays (PAM-R) identified genes corresponding with protection. Gene Set Enrichment Analysis (GSEA) identified sets of genes associated with protection after the third immunization, before challenge.

Publication Title

Expression of genes associated with immunoproteasome processing of major histocompatibility complex peptides is indicative of protection with adjuvanted RTS,S malaria vaccine.

Sample Metadata Fields

Specimen part

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accession-icon GSE21671
Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

STAT3, an essential transcription factor with pleiotropic functions, plays critical roles in the pathogenesis of autoimmunity. Despite recent data linking STAT3 with inflammatory bowel disease, exactly how it contributes to chronic intestinal inflammation is not known. Using a T cell transfer model of colitis we found that STAT3 expression in T cells was essential for the induction of both colitis and systemic inflammation. STAT3 was critical in modulating the balance of T helper 17 (Th17) and regulatory T (Treg) cells, as well as in promoting CD4+ T cell proliferation. We used chromatin immunoprecipitation and massive parallel sequencing (ChIP-Seq) to define the genome-wide targets of STAT3 in CD4+ T cells. We found that STAT3 bound to multiple genes involved in Th17 cell differentiation, cell activation, proliferation and survival, regulating both expression and epigenetic modifications. Thus, STAT3 orchestrates multiple critical aspects of T cell function in inflammation and homeostasis.

Publication Title

Diverse targets of the transcription factor STAT3 contribute to T cell pathogenicity and homeostasis.

Sample Metadata Fields

Specimen part

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accession-icon SRP076710
Biotin tagging of MeCP2 reveals contextual insights into the Rett syndrome transcriptome
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Mutations in MECP2 cause Rett syndrome (RTT), a X-linked neurological disorder characterized by the regressive loss of neurodevelopmental milestones and acquired intellectual disability and motor impairments. However, the cellular heterogeneity of the mammalian brain impedes our understanding of how MECP2 mutations disrupt neuronal function and contribute to RTT. In response, we developed cell type-specific biotin tagging in mice bearing RTT-associated mutations and profiled nuclear transcriptomes in WT and mutant neurons. Although individual gene expression changes are largely specific to each mutation and cell type, higher-level transcriptional features remain conserved and correlate with RTT phenotypic severity. Furthermore, subcellular RNA populations support post-transcriptional compensation as a basis for the upregulation of long genes previously reported in RTT mutant neurons. Finally, we overcame the genetic mosacism associated with female RTT mouse models and identified functionally distinct gene expression changes in neighboring WT and mutant neurons, which altogether provide key contextual insights into RTT. Overall design: Nuclear total RNA-seq of two types of neurons of male and female RTT mice and GRO-seq of the cortex

Publication Title

Biotin tagging of MeCP2 in mice reveals contextual insights into the Rett syndrome transcriptome.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon GSE42853
Distinct gene expression profiles associated with the susceptibility of pathogen-specific CD4 T cells to HIV-1 infection
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of global gene expression profiles of flow cytometry-sorted, different pathogen-specific CD4+ T cell populations from the same peripheral blood mononuclear cells (PBMC), to identify molecular parameters that regulate differential susceptibilities of these CD4+ T cells to HIV infection. The results reveal distinct gene expression profiles between CMV-specific and tetanus toxoid/Candida-specific CD4+ T cells that involved selective upregulation of comprehensive innate antiviral

Publication Title

Distinct gene-expression profiles associated with the susceptibility of pathogen-specific CD4 T cells to HIV-1 infection.

Sample Metadata Fields

Specimen part

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

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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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