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accession-icon GSE48350
Alzheimer's Disease Dataset
  • organism-icon Homo sapiens
  • sample-icon 246 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This dataset contains microarray data from normal controls (aged 20-99 yrs) and Alzheimer's disease cases, from 4 brain regions: hippocampus, entorhinal cortex, superior frontal cortex, post-central gyrus. Changes in expression of synaptic and immune related genes were analyzed, investigating age-related changes and AD-related changes, and region-specific patterns of change.

Publication Title

Gene expression changes in the course of normal brain aging are sexually dimorphic.

Alternate Accession IDs

E-GEOD-48350

Sample Metadata Fields

Sex, Subject

View Samples
accession-icon GSE11882
Gene expression changes in the course of normal brain aging are sexually dimorphic
  • organism-icon Homo sapiens
  • sample-icon 168 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This dataset of cognitively normal controls is a subset of the GSE48350 dataset, which additionally contains microarray data from AD brains.

Publication Title

Gene expression changes in the course of normal brain aging are sexually dimorphic.

Alternate Accession IDs

E-GEOD-11882

Sample Metadata Fields

Sex, Subject

View Samples
accession-icon SRP059963
Investigation about Monocytes in metastatic breast cancer patients under chemotherapy +/- Avastin
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The goal of this study was to determine if blood circulating monocytes of metastatic breast cancer patient would express a different activation profile compared to healthy donors, in order to use this specific changesas biomarkers to monitor then response to therapy Overall design: CD11b+ cells were extracted from all blood of 4 healthy donors and 4 metastatic breast cancer patients using magnetic beads separation (Miltenyi). CD11b+ cells were then lysed and mRNA was extracted to perform RNASeq.

Publication Title

Bevacizumab specifically decreases elevated levels of circulating KIT+CD11b+ cells and IL-10 in metastatic breast cancer patients.

Alternate Accession IDs

GSE70404

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE21142
Tobacco smoking transcriptional imprinting contributes to urothelial cancer
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Smoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours.

Publication Title

New insights into the influence of cigarette smoking on urothelial carcinogenesis: smoking-induced gene expression in tumor-free urothelium might discriminate muscle-invasive from nonmuscle-invasive urothelial bladder cancer.

Alternate Accession IDs

E-GEOD-21142

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE73355
The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The goal of this study was to assess whether the presence of HLA-B*35 contributes to activation of ER stress/UPR and inflammation in lcSScPAH PBMC.

Publication Title

The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.

Alternate Accession IDs

E-GEOD-73355

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE49373
Expression data from the lungs of Scnn1b-Transgenic and wild-type mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Airway mucus obstruction triggers macrophage activation and MMP12-dependent emphysema

Publication Title

Airway mucus obstruction triggers macrophage activation and matrix metalloproteinase 12-dependent emphysema.

Alternate Accession IDs

E-GEOD-49373

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE47504
Gene expresssion changes in pancreatic islets of 11 weeks old IKK2-CApdx-1 mice compared to control and Pdx-1+/- mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Canonical IKK/NF-B signaling is a master regulator of inflammation and innate immunity and has been implicated in the pathogenesis of T1D. To investigate the impact of NF-B activation on -cell homeostasis and diabetes development, we generated a transgenic gain-of-function mouse model allowing conditional NF-B activation via expression of IKK2-CA (constitutively active IKK2 allele) in -cells using the tetracycline-regulated gene expression system. Pdx-1-tTA (knockin model generating Pdx-1 haploinsufficiency) driver mice were used for -cell specific transgene expression. Double transgenic IKK2-CA-pdx-1 mice develop a full-blown immune-mediated diabetes.To identify gene expression changes underlying this diabetes development pancreatic islets of diabetic IKK2-CA-Pdx-1, PDX-1 +/- and control mice were prepared and isolated total RNA was used for microarray analysis.

Publication Title

Long-term IKK2/NF-κB signaling in pancreatic β-cells induces immune-mediated diabetes.

Alternate Accession IDs

E-GEOD-47504

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE25182
tTA/TDP Mice Expression Array
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Transgenic (Tg) mice expressing nuclear or cytoplasmic human TDP-43 were generated.

Publication Title

Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in mice.

Alternate Accession IDs

E-GEOD-25182

Sample Metadata Fields

Sex

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accession-icon GSE13162
Expression data from postmortem human brain samples with and without FTLD-U
  • organism-icon Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

FTLD-U is the most common pathological correlate of the neurodegenerative dementia frontotemporal dementia

Publication Title

Variations in the progranulin gene affect global gene expression in frontotemporal lobar degeneration.

Alternate Accession IDs

E-GEOD-13162

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP130961
RNA sequencing of sorted microglia from NEFH-tTa/tetO-hTDP43 transgenic mouse whole spinal cord
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Microglia are the resident myeloid-lineage cells in the central nervous system. Despite myriad observations of microglia associated with various tissue pathologies in degenerative disease, their function in and contributions to the pathophysiological processes remain unclear. It is particularly uncertain whether microglia act harmfully to contribute to worsening of degeneration, act beneficially to combat disease-related dysfunction, or perform functions that result in both outcomes. In this dataset, we report RNA sequencing results from mice that undergo inducible ALS/FTLD-like degeneration and subsequent recovery. The goals were to identify whether microglia show transcriptional signatures commensurate with the disease stage or if they remain constant throughout. Additionally, we sought to understand whether there was a particular transcriptional or functional signature associated with functional recovery in the mice. The latter could lead to an understanding of how microglia may be targeted to combat disease and enhance recovery following or during degeneration. Overall design: mRNA profiles from microglia sorted from whole-spinal cord taken from doxycycline (DOX) inducible NEFH-tTa/tetO-208-hTDP43 (rNLS8, (+/+)) mice. In these mice, removal of doxycycline from the diet (DOX-OFF) induces transgenic expression and degeneration and reintroduction (DOX-ON) suppresses expression and enables recovery. We report profiles from rNLS8 mice that were DOX-OFF for 2 weeks (N=8) or 6 weeks (N=7), or DOX-OFF for 6 weeks followed by DOX-ON for 1 week (N=9). We also report profiles from control samples that include: rNLS8 mice that were DOX-ON for 6 weeks (N = 6) as asymptomatic genetic controls and WT (-/-) littermates that were DOX-OFF for 2 weeks (N=4), 6 weeks (N=1), or DOX-OFF for 6 weeks followed by 1 week DOX-ON (N=3) as asymptomatic doxycycline controls.

Publication Title

Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy.

Alternate Accession IDs

GSE109171

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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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