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accession-icon GSE32387
Prolactin stimulation of parathyroid adenomas
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Primary hyperparathyroidism is a common endocrine disorder frequently affecting postmenopausal women. In this study we have investigated expression of the prolactin receptor (PRLr) in a panel of 37 sporadic parathyroid tumours, as well as functionality in vitro in cultured parathyroid tumour cells. High levels of the prolactin receptor gene (PRLR) transcripts were demonstrated in parathyroid tissues as compared to other reference tissues and breast cancer cells. PRLr products of 60/70 kDa were highly expressed in all parathyroid tumours. In addition varying levels of the 80 kDa PRLr isoform, with known proliferative activity, were demonstrated. In parathyroid tumours PRLr immunoreactivity was observed in cytoplasm in all cases and in addition in the plasma membrane (n = 12) or enlarged lysosomes (n = 4). In normal parathyroid rim PRLr was expressed in cytoplasm and granulae. In in vitro studies of short-term cultured human parathyroid tumour cells prolactin stimulation was associated with transcriptional changes in JAK/STAT, RIG-I like receptor and type II interferon signaling pathways as documented by gene expression profiling. Moreover, PRLR gene expression in parathyroid tumors was significantly inversely correlated with plasma total Ca2+ levels. In conclusion, the prolactin receptor was found highly abundant in human parathyroid gland, parathyroid tumours, correlated with patient Ca2+ levels and functionally responsive to physiological levels of prolactin. These findings suggest a role for the prolactin receptor in human parathyroid adenomas.

Publication Title

Prolactin receptor in primary hyperparathyroidism--expression, functionality and clinical correlations.

Sample Metadata Fields

Specimen part

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accession-icon GSE70362
Gene Expression Profiling Identifies Interferon Signalling Molecules and IGFBP3 in Human Degenerative Annulus Fibrosus
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Low back pain is a major cause of disability especially for people between 20 and 50 years of age. As a costly healthcare problem, it imposes a serious socio-economic burden. Current surgical therapies have considerable drawbacks and fail to replace the normal disc in facilitating spinal movements and absorbing load. Therefore, the focus of regenerative medicine is on identifying biomarkers and signalling pathways to improve our understanding about the cascades of disc degeneration and allow for the design of specific therapies. We hypothesized that comparing microarray profiles from degenerative and non-degenerative discs will lead to the identification of dysregulated signalling and pathophysiological targets. Microarray data sets were generated from human annulus fibrosus cells and analysed using IPA ingenuity pathway analysis system. Gene expression values were validated by qRT-PCR, and respective proteins were identified by immunohistochemistry. Microarray analysis revealed 17 dysregulated molecular markers and various dysregulated cellular functions, including cell proliferation and inflammatory response, in the human degenerative annulus fibrosus. The most significant canonical pathway induced in degenerative annulus fibrosus was found to be the interferon signalling pathway. In conclusion, this study indicates interferon-alpha signalling pathway activation with IFIT3 and IGFBP3 up-regulation which may affect cellular function in human degenerative disc.

Publication Title

Gene Expression Profiling Identifies Interferon Signalling Molecules and IGFBP3 in Human Degenerative Annulus Fibrosus.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE56139
Gene expression profiling from MCF7
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

proliferative effect in MCF7 cells.

Publication Title

Estrogen Receptor β as a Therapeutic Target in Breast Cancer Stem Cells.

Sample Metadata Fields

Cell line

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accession-icon GSE47568
Gene expression changes in Apc-mutant mouse intestinal organoids with and without deleting the Prox1 transcription factor
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We isolated and selected intestinal adenoma organoids from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox mice and added tamoxifen to induce the deletion of the Apc and Prox1 genes in the intestinal epitheliul ex vivo. Microarray experiments were carried out 7 days after the addition of tamoxifen.

Publication Title

Prox1 promotes expansion of the colorectal cancer stem cell population to fuel tumor growth and ischemia resistance.

Sample Metadata Fields

Specimen part

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accession-icon GSE35094
Apc, Kras, and TGFbeta in intestinal organoids
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Oncogenic mutations in intestinal adenomas regulate Bim-mediated apoptosis induced by TGF-β.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE35093
The effect of TGF-beta in Apc-mutated mouse intestinal organoids
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Intestinal crypts isolated from Apcflox/flox; villin-CreERT mice were treated with Tamoxifen to induce the deletion of Apc. Tamoxifen-treated organoids were selected in the absence of Wnt agonists and then treated with TGF-beta.

Publication Title

Oncogenic mutations in intestinal adenomas regulate Bim-mediated apoptosis induced by TGF-β.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE147383
Gene expression data for human intervertebral discs
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The human intervertebral disc (IVD) is a complex and dynamic structure that functions to provide spinal stability, mobility and flexibility. It comprises three main compartments: 1) a water-rich central compartment called the nucleus pulposus (NP), which is enveloped by 2) the annulus fibrosus (AF) and sandwiched between 3) two cartilaginous endplates (EP) from which the IVD gains its nutrition and provides a means to get rid of metabolic waste.

Publication Title

DIPPER, a spatiotemporal proteomics atlas of human intervertebral discs for exploring ageing and degeneration dynamics.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE91393
Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.

Sample Metadata Fields

Specimen part

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accession-icon GSE91392
Human expression data from Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin.
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

The cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy.

Publication Title

Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.

Sample Metadata Fields

Specimen part

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accession-icon GSE91391
Mouse expression data from Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy.

Publication Title

Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.

Sample Metadata Fields

Specimen part

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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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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