Human prolactinoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE36314 | GEO | 2012/03/08
SECONDARY ACCESSION(S): PRJNA153353
REPOSITORIES: GEO
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Project description:Human prolactinomas (n=4, 3 males and 1 female) were obtained during trans-sphenoidal surgery as part of an ongoing accession of human pituitary tumors. The study was approved Institutional Review Board (IRB) of Emory University, and informed consent obtained for all subjects. Tumors were microdissected and removed using the surgical microscope, rinsed in sterile saline, snap-frozen in liquid nitrogen, and stored (-80 ℃) until analysis. Each tumor fragment was confirmed independently by a neuropathologist by histology and immunohistochemistry prior to molecular analysis. Three normal pituitary glands from cadavers were obtained from the National Resource Center (NDRI, www.ndriresource.org). Each human tissue sample was analyzed using Affymetrix Human Genome U95Av2 arrays. 4 prolactinoma and 3 normal pituitaries
2012-03-08 | E-GEOD-36314 | biostudies-arrayexpress
Project description:Analysis the different gene expression of prolactinomas and normal pituitary tissues. Prolactinoma is a benign pituitary tumor that produces excessive prolactin resulting in hyperprolactinemia and another disease.Tissues were microdissected and removed using the surgical microscope, rinsed in sterile saline, snap-frozen in liquid nitrogen, and stored (-80 ℃) until analysis. Results provide insight into understanding the difference of gene expression in prolacinomas.
2018-09-03 | GSE119063 | GEO
Project description:Pituitary adenomas cause significant endocrine and mass-related morbidity. Not much is known about mechanisms underlying pituitary tumor pathogenesis.We searched for a side population (SP) in pituitary tumor, representing cells with high efflux capacity and potentially enriching for cancer/tumor stem cells (CSC/TSC). Human pituitary adenomas contain a SP irrespective of hormonal phenotype. This adenoma SP, as well as the further purified SP (pSP) depleted from endothelial and immune cells, enriches for cells that express ‘tumor stemness’ markers and signaling pathways, including epithelial-mesenchymal transition (EMT)-linked factors. The adenomas were found to contain self-renewing sphere-forming cells, considered a property of TSC. The sphere-initiating cells were retrieved in the pSP.Because benign pituitary adenomas do not grow in vitro and failed to expand in immunodeficient mice, the pituitary tumor cell line AtT20 was further used. We identified a SP in this cell line and found it more tumorigenic than the main population (MP). Of the two EMT-regulatory pathways tested, inhibition of Cxcr4 signaling reduced EMT-linked cell motility in vitro as well as xenograft tumor growth, whereas activation of TGFβ had no effect.The tumor pSP showed upregulated expression of the pituitary stem cell marker SOX2. Pituitaries from dopamine receptor D2 knockout (Drd2-/-) mice bearing prolactinomas, contain more pSP, Sox2+ and colony-forming cells than wildtype glands.In conclusion, we detected a SP in pituitary tumors and identified TSC-associated characteristics. Our study may contribute to a better understanding of pituitary tumor pathogenesis and lead to new therapeutic targets. We determined gene expression profiles for 9 human pituitary adenoma samples (5 x NF-A; 4 x GH-A). The samples were obtained immediately after transsphenoidal resection (by the neurosurgeon Dr. van Loon, Division Neurosurgery, University Hospitals Leuven). Informed consent was received from the patients. Hormonal phenotype was determined by the Department of Imaging and Pathology (University Hospitals Leuven). For each sample, total SP and MP cells were sorted by FACS. Separate assays were run subsequently for the two fractions. As such we present data from 18 microarrays.
2015-08-04 | E-GEOD-62866 | biostudies-arrayexpress
Project description:Whole peripheral blood samples collected into Paxgene tubes from 338 adult participants in the Emory University Cardiovascular Biobank, in Midtown Atlanta. The sample is of mixed cardiovascular function diversity, and is part of a survey of the impact of status of cardiovascular disease on gene expression and clinical attributes. Sample annotations only include gender and proofed ethnicity for purposes of IRB, as well as technical features of the study (plate, phase of study, and RNA quality RIN score).
2014-07-01 | GSE49925 | GEO
Project description:Whole peripheral blood samples collected into Paxgene tubes from 338 adult participants in the Emory University Cardiovascular Biobank, in Midtown Atlanta. The sample is of mixed cardiovascular function diversity, and is part of a survey of the impact of status of cardiovascular disease on gene expression and clinical attributes. Sample annotations only include gender and proofed ethnicity for purposes of IRB, as well as technical features of the study (plate, phase of study, and RNA quality RIN score). 338 individuals in the Emory Cardiovascular Biobank in Midtown Atlanta., 219 men and 119 women. The age of individulas were between 26 and 85 (mean 62). 333 Caucasian (CAU), 4 African American (AFA), 1 South Asian (SAS).
2014-07-01 | E-GEOD-49925 | biostudies-arrayexpress
Project description:Pituitary adenomas cause significant endocrine and mass-related morbidity. Not much is known about mechanisms underlying pituitary tumor pathogenesis. We searched for a side population (SP) in pituitary tumor, representing cells with high efflux capacity and potentially enriching for cancer/tumor stem cells (CSC/TSC). Human pituitary adenomas contain a SP irrespective of hormonal phenotype. This adenoma SP, as well as the further purified SP (pSP) depleted from endothelial and immune cells, enriches for cells that express ‘tumor stemness’ markers and signaling pathways, including epithelial-mesenchymal transition (EMT)-linked factors. The adenomas were found to contain self-renewing sphere-forming cells, considered a property of TSC. The sphere-initiating cells were retrieved in the pSP. Because benign pituitary adenomas do not grow in vitro and failed to expand in immunodeficient mice, the pituitary tumor cell line AtT20 was further used. We identified a SP in this cell line and found it more tumorigenic than the main population (MP). Of the two EMT-regulatory pathways tested, inhibition of Cxcr4 signaling reduced EMT-linked cell motility in vitro as well as xenograft tumor growth, whereas activation of TGFβ had no effect. The tumor pSP showed upregulated expression of the pituitary stem cell marker SOX2. Pituitaries from dopamine receptor D2 knockout (Drd2-/-) mice bearing prolactinomas, contain more pSP, Sox2+ and colony-forming cells than wildtype glands. In conclusion, we detected a SP in pituitary tumors and identified TSC-associated characteristics. Our study may contribute to a better understanding of pituitary tumor pathogenesis and lead to new therapeutic targets. We determined gene expression profiles for 5 human pituitary adenoma samples (all NF-A type). The samples were obtained immediately after transsphenoidal resection (by the neurosurgeon Dr. van Loon, Division Neurosurgery, University Hospitals Leuven). Informed consent was received from the patients. Hormonal phenotype was determined by the Department of Imaging and Pathology (University Hospitals Leuven). For each sample, CD31¯/CD45¯ SP (purified SP or pSP) and pMP cells were sorted by FACS. Separate assays were run subsequently for the two fractions. As such we present data from 10 microarrays.
2015-08-04 | E-GEOD-62870 | biostudies-arrayexpress
Project description:miRNAs expression is known to be deregulated in many types of cancer leading to suspect them implication in crucial steps occurring during tumor progression and maybe as potential driving genes. In this study we tried to decipher the place of miRNA in the hierarchical events cascade occurring in prolactinoma-tumours progression toward malignancy by using an integrative genomic approach performed on the same samples associating global miRNA expression, transcriptomic, DNA structure and methylation analyses. By this approach, we observed the down-regulation of 3 miRNAs (miR-183, miR-98, and miR-744) in A vs. NA tumors. MiR-98 and miR-744 were demonstrated to regulate respectively E2F2 and TGFB1 which are up-regulated in the A vs. NA prolactinomas. Moreover we demonstrated that KIAA0101 is a new target of miR-183 and that miR-183 is regulated by the transcription factor ETS2. KIAA0101 is up-regulated in the A vs. NA prolactinomas. KIAA0101, E2F2 and TGFB1 are interconnected in a pathway controlling cell proliferation and invasion that is over-activated in A PRL tumors. Thus the down-regulation of these three miRNAs is involved in the tumoral progression of human prolactinoma towards aggressiveness. The integrative genomic approach used here allowed us to propose a model of PRL tumoral progression towards aggressiveness. Moreover it revealed the potential of integrative genomic strategy applied in the same human tumors to identify the molecular mechanisms responsible for tumor progression even from a small cohort of patients. miRNA signatures was assessed on 4 aggressive, 8 non-aggressive human prolactin secreting pituitary tumors and 1 normal pituitary for data normalization.
2015-05-01 | E-GEOD-46294 | biostudies-arrayexpress
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2021-07-01 | GSE154446 | GEO
Project description:Array CGH analysis of Helicobacter pylori strains isolated from a North American cohort of symptomatic pediatric patients. Keywords: genotyping_design A genotyping experiment design type classifies an individual or group of individuals on the basis of alleles, haplotypes, SNP's. Patients enrolled under Benjamin Gold's Emory IRB protocol. Initial strain isolation from antral biopsies performed at Emory and culture sweeps sent to FHCRC (Seattle) for analysis. Single colony isolates (4) from each patient antral biopsy were isolated and profiled using RAPD. A single clone of each RAPD type detected in each patient (1-2) were analyzed on duplicate arrays. For analysis 500 ng of genomic DNA of each test strain was labeled with Cy5 and 500 ng of genomic DNA of a reference sample (equimolar mix of 26695 and J99) was labeled with Cy3. Strains identified as Em-patient#-clone#.
2009-11-04 | E-GEOD-13317 | biostudies-arrayexpress
Project description:Pituitary adenomas cause significant endocrine and mass-related morbidity. Not much is known about mechanisms underlying pituitary tumor pathogenesis. We searched for a side population (SP) in pituitary tumor, representing cells with high efflux capacity and potentially enriching for cancer/tumor stem cells (CSC/TSC). Human pituitary adenomas contain a SP irrespective of hormonal phenotype. This adenoma SP, as well as the further purified SP (pSP) depleted from endothelial and immune cells, enriches for cells that express ‘tumor stemness’ markers and signaling pathways, including epithelial-mesenchymal transition (EMT)-linked factors. The adenomas were found to contain self-renewing sphere-forming cells, considered a property of TSC. The sphere-initiating cells were retrieved in the pSP. Because benign pituitary adenomas do not grow in vitro and failed to expand in immunodeficient mice, the pituitary tumor cell line AtT20 was further used. We identified a SP in this cell line and found it more tumorigenic than the main population (MP). Of the two EMT-regulatory pathways tested, inhibition of Cxcr4 signaling reduced EMT-linked cell motility in vitro as well as xenograft tumor growth, whereas activation of TGFβ had no effect. The tumor pSP showed upregulated expression of the pituitary stem cell marker SOX2. Pituitaries from dopamine receptor D2 knockout (Drd2-/-) mice bearing prolactinomas, contain more pSP, Sox2+ and colony-forming cells than wildtype glands. In conclusion, we detected a SP in pituitary tumors and identified TSC-associated characteristics. Our study may contribute to a better understanding of pituitary tumor pathogenesis and lead to new therapeutic targets.
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