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accession-icon E-MEXP-1074
Transcription profiling by array of excisional biopsy wounds from young and old human subjects to measure the influence of age on cutaneous wound healing
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The aim of this experiment was measure the influence of age on cutaneous wound healing using human subjects. Increaded age has been associated with delayed wound healing in mouse models and in humans. Gene expression was compared between excisional biopsy wounds from young and old subjects.

Publication Title

Estrogen, not intrinsic aging, is the major regulator of delayed human wound healing in the elderly.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon E-MEXP-1232
Transcription profiling by array of skin wound samples from rats treated with the 5alpha-reductase inhibitor MK-434
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

The present study aimed to delineate the central mechanisms by which androgens delay wound repair. Blocking the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) by 5alpha-reductase limits its ability to impair skin wound healing, suggesting that DHT is a more potent inhibitor of repair than is testosterone. This study aims to identify, through transcription profiling, potential mechanisms by which the 5alpha-reductase inhibitor MK-434 modulates repair. Microarray analysis of wound RNA samples from rats in which the transformation of testosterone to DHT is prevented has identified biological processes and key individual genes through which DHT may contribute to the altered healing profile in such animals. These include genes with putative roles in wound contraction and re-epithelialization.

Publication Title

5alpha-dihydrotestosterone (DHT) retards wound closure by inhibiting re-epithelialization.

Sample Metadata Fields

Sex, Age, Specimen part, Compound

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accession-icon SRP133401
Expression profiling by RNA-Seq of breast cancer samples from patients in walnut-consuming and control groups
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

Consumption of walnuts has slowed breast cancer growth and/or reduced the risk of breast cancer in mice. The significantly reduced mean tumor size or numbers of tumors was associated with changing the expressions of many genes that are associated with cancer growth, survival and metastasis. Many women treated for breast cancer are interested in reducing the risk for recurrence. The study was a non-placebo, two-arm, clinical trial. Women with lumps large enough for research and pathology biopsies were recruited to the trial. One or two additional biopsies were taken for gene expression analyses using next generation RNA Sequencing methods. The subjects randomized to the walnut group immediately began to consume 2 ounces of walnuts per day until follow-up surgery, if surgery were needed. At follow up surgery, additional biopsies were taken from the surgically removed, cancerous tissue for additional gene expression analyses. Changes in gene expression compared to baseline were determined in tumors of each individual woman in walnut-consuming and control groups. Overall design: Gene expression profiles of two samples from each of ten breast cancer patients were obtained via RNA-Seq in a 2x50bp paired-end design. The first sample was obtained from biopsy; the second sample was taken at the time of surgery 2-3 weeks later. Five patients consumed two one-ounce packets of walnuts daily between the biopsy and surgery, while the other five remained on their regular diet.

Publication Title

Dietary walnut altered gene expressions related to tumor growth, survival, and metastasis in breast cancer patients: a pilot clinical trial.

Sample Metadata Fields

Specimen part, Subject

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accession-icon E-MEXP-209
Transcription profiling of wounds from ovariectomized MIF null mice and controls to investigate the role of MIF during wound healing using BALB/C MIF null mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.

Publication Title

Macrophage migration inhibitory factor: a central regulator of wound healing.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE109632
Expression data from human hair follicles (ex vivo) incubated with cyclosporine A and vehicle control
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Since hair growth disorders can carry a major psychological burden, more effective human hair growth-modulatory agents need to be urgently developed. Here, we used the hypertrichosis-inducing immunosuppressant, cyclosporine A (CsA), as a lead compound to identify new hair growth-promoting targets. Through microarray analysis we identified the Wnt inhibitor, SFRP1, as being downregulated in the dermal papilla (DP) of CsA-treated human scalp hair follicles (HFs) ex vivo. Therefore, we further investigated the function of SFRP1 using a pharmacological approach and found that SFRP1 regulates intrafollicular canonical Wnt/-catenin activity through inhibition of Wnt ligands in the human hair bulb. Conversely, inhibiting SFRP1 activity through the SFRP1 antagonist, WAY-316606, enhanced hair shaft production, hair shaft keratin expression and inhibited spontaneous HF regression (catagen) ex vivo. Collectively, these data (a) identify Wnt signaling as a novel, non-immune-inhibitory CsA target; (b) introduce SFRP1 as a physiologically important regulator of canonical -catenin activity in a human (mini-)organ; and (c) demonstrate WAY-316606 to be a promising new promoter of human hair growth. Since inhibiting SFRP1 only facilitates Wnt signaling through ligands that are already present, this ligand-limited therapeutic strategy for promoting human hair growth may circumvent potential oncological risks associated with chronic Wnt over-activation.

Publication Title

Identifying novel strategies for treating human hair loss disorders: Cyclosporine A suppresses the Wnt inhibitor, SFRP1, in the dermal papilla of human scalp hair follicles.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP167389
Gene expression profiles of isogenic single-cell derived clones of BRAF-mutated SK-MEL-5 melanoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 3000

Description

We recently reported that single-cell derived isogenic subclones of SKMEL5 cells have differential initial sensitivity to BRAF-inhibitors. In order to probe differences among these subclones, we selected three subclones with unique drug responses: progressing (SK-MEL-5 SC10), stationary (SK-MEL-5 SC07), and regressing (SK-MEL-5 SC01) and performed RNASeq. This study examines differentially expressed genes (DEGs) among the subclones to identify the molecular basis for initial differences in drug sensitivity. Overall design: Transcriptomics analysis between single-cell derived isogenic subclones of BRAF-mutated melanoma cell line, SK-MEL-5

Publication Title

A Nonquiescent "Idling" Population State in Drug-Treated, BRAF-Mutated Melanoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE45437
Expression data from paediatric ependymoma short-term cell cultures
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours.

Publication Title

Epigenetic genome-wide analysis identifies BEX1 as a candidate tumour suppressor gene in paediatric intracranial ependymoma.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE53335
Regulation of inducible genes in epithelial to mesenchymal transition by chromatinized PKC-theta
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE53266
Gene expression changes in a breast cancer stem cell model.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.

Publication Title

Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon E-MEXP-558
Transcription profiling by array of connexin30 knock-out mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Effect of the ablation of connexin 30 in the stria vascularis

Publication Title

Connexin30 deficiency causes instrastrial fluid-blood barrier disruption within the cochlear stria vascularis.

Sample Metadata Fields

Age, Specimen part, Disease, Time

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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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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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