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accession-icon GSE106656
Expression data from stomach biopsies with gastritis and intestinal metaplasia lesions
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Helicobacter pylori is a well-recognized bacterium associated with the development of several histopathological lesions in the stomach. The chronic infection produces an inflammatory lesion known as gastritis. This lesion can later progress to more serious lesions such as intestinal metaplasia. Some attempts in the transcriptome of these conditions have been made; these however, have yielded limited information. Given the potential of high-throughput technologies for understanding biological processes altered and in the description of biomarkers of disease, we performed a genome-wide gene expression analysis in gastric biopsies. The aim of this study was to describe the altered molecular mechanism and potential biomarkers of follicular gastritis, chronic gastritis and intestinal metaplasia, through the identification of characteristic gene expression profiles in each histopathological lesion. The exploratory set comprised twenty-one biopsies from patients with follicular gastritis (n=7), chronic gastritis (n=7), and intestinal metaplasia (n=7), which were analyzed by whole-genome gene expression microarrays. The enrichment analyses and functional annotation of genes using computational tools were performed. The bioinformatics data of the same 21 biopsies were validated by real time PCR analysis while 79 FFPE samples were analyzed by immunohistochemistry.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age

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accession-icon GSE108998
Allopregnanolone alters the gene expression profile of human glioblastoma cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Glioblastomas (GBM) are one of the most frequent and aggressive brain tumors. In these malignancies, progesterone (P4) promotes proliferation, migration, and invasion. The P4 metabolite allopregnanolone (3-THP) similarly promotes cell proliferation in the U87 human GBM cell line.

Publication Title

Allopregnanolone Alters the Gene Expression Profile of Human Glioblastoma Cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE94718
EFFECTS OF IDURSULFASE TREATMENT ON EXTRACELLULAR MATRIX COMPONENTS, INTRACELLULAR SIGNALING AND PROLIFERATION/DIFFERENTIATION REGULATION IN CALVARIA-DERIVED BONE TISSUE OF APERT SYNDROME PATIENTS
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Experimental in vtiro approach to molecular pathways implicated in Apert Syndromes craniosynostosis through transcriptomics techniques. FGFR2 activation requires a tridimensional configuration between ligand, receptor and heparan sulfate(HS). Mutations in the extracellular region of this receptor affect the balance between proliferation and differentiation of osteoprogenitor cells, leading to craniosynostosis as Apert Syndrome (AS). We postulate that the degradation of HS in periosteal tissue in patients with AS can modify the gene expression profile and modulate cell behavior. Based on previous evidence we propose that the treatment with an enzyme that degrades HS, as Idursulfase, in periosteal tissue of patients with AS, could be affect the formation of the ternary complex (FGF / FGFR / HS), triggering changes in gene profiles expression in several molecular pathways, regarding their basal state with the mutated receptor.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon GSE10820
Search for New Biomarkers for the Monitoring of the Minimal Residual Disease of the Acute Lymphoblastic Leukemia.
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The main goal of the research was to find some new biomarkers for the monitoring of the Minimal Residual Disease in Acute Lymphoblastic Leukemia patients.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age

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accession-icon GSE29245
Amplified genes are not necessarily over expressed, they can be unchanged or down regulated in cervical cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Mapping 50K Hind240 SNP Array (mapping50khind240), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE29216
Amplified genes are not necessarily over expressed, they can be unchanged or down regulated in cervical cancer cell lines [expression array data]
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Mapping 50K Hind240 SNP Array (mapping50khind240)

Description

Several copy number altered regions (CNA) have been identified in the genome of cervical cancer, especially amplifications of 3q and 5p. However, the contribution of those alterations to cervical carcinogenesis is still a matter of debate, since genome-wide, there is a lack of correlation between CNAs and gene expression. In this study, we investigated whether the CNAs in cell lines (CaLo, CasKi, HeLa, SiHa), at a gene-by-gene level, are related to changes in gene expression. On average 19.2% of the whole genome of cell lines had CNA. However, only 2.4% consisted of minimal recurrent regions (MRR), common to all cell lines. Whereas 3q had just some sparse common gains (13%), 5p was entirely duplicated recurrently. Genome-wide, only 11% of genes located in CNAs changed gene expression. In contrast, the rate increased over 3 fold times in MRRs. Chr 5p was confirmed entirely amplified by FISH. In spite of this, at most 32.9% of the explored genes in 5p (n=202) were de-regulated. In 3q, the rate was just 11.8%. Even in 3q26, which had five MRRs and 38.7% of SNPs was gained recurrently, the rate rose slightly to 13.6% (10 out of 73). Interestingly, up to 16% of de-regulated genes in 5p and 80% in 3q26 were down-regulated, suggesting additional factors are involved in gene repression. The de-regulated genes in 3q and 5p were found in clusters, suggesting local chromatin factors may also influence gene expression. In regions amplified discontinuously, the rate of down-regulated genes rose steadily as the number of amplified SNPs increased (p<0.01, Spearman's correlation). This suggests partial gene amplification as a mechanism of silencing gene expression. Additional genes were identified up- or down-regulated in 5p and 3q, which could be involved in cervical carcinogenesis, especially implicated in apoptosis. Those include CLPTM1L, AHRR, PDCD6 and DAP in 5p and TNFSF10 and ECT2 in 3q. Overall, the gene expression and copy number profiles suggest other factors, like epigenetic or chromatin domains, may influence gene expression within the entirely amplified genome segments. Further studies are needed to elucidate how these mechanisms regulate gene expression.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Cell line

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accession-icon GSE46988
Expression data from rat spinal cord injury and mesenchymal stromal cells (MSC) or olfactory ensheathing cells (OEC) transplantation
  • organism-icon Rattus norvegicus
  • sample-icon 52 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.1 ST Array (ragene11st)

Description

We analyzed the changes in the spinal cord transcriptome after a spinal cord contusion injury and MSC or OEC transplantation. The cells were injected immediately or 7 days after the injury. The mRNA of the spinal cord injured segment was extracted and analyzed by microarray at 2 and 7 days after cell grafting.

Publication Title

Gene expression changes in the injured spinal cord following transplantation of mesenchymal stem cells or olfactory ensheathing cells.

Sample Metadata Fields

Treatment

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accession-icon GSE29570
The mtDNA Amerindian Haplogroup B2 enhances the risk for Cervical Cancer of HPV: de-regulation of mitochondrial genes may be involved.
  • organism-icon Homo sapiens
  • sample-icon 61 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Although Human papillomavirus infection is the main causal factor for cervical cancer (CC), there is data suggesting genetic factors could modulate the risk and progression of CC. Sibling studies suggest that maternally inherited factors could be involved in CC. To assess whether mitochondrial DNA (mtDNA) polymorphisms are associated to cervical cancer, HPV infection and HPV types, a case-control study was performed in the Mexican mestizo population. The polymorphism of mtDNA D-Loop was investigated in 187 cervical cancer patients and 270 healthy controls. D-loop was amplified from a blood DNA sample and analyzed by sequencing. HPV was detected and typed in cervical scrapes from both groups. mtDNA polymorphisms were compared in the whole samples and stratified by HPV types. The expression of 29 mitochondrial genes was analyzed in a subset of 45 tumor biopsies using the expression microarray ST1.0. The Amerindian haplogroup B2 increased the risk for CC (OR=1.6, 95% CI: 1.05-2.58) and showed an additive effect of 36% over the risk conferred by the HPV (OR=153, 95% CI: 65.4-357.5). The frequency of HPV 16, 18, 31 and 45 in cancer samples was similar in all haplogroups but one (D1). It showed a very low frequency of HPV16, any HPV18 and high frequency of HPVs 31, 45 and other types. Two mtDNA genes (MT-TD, MTTK) could be involved in the increased risk conferred by the haplogroup B2, since they were up-regulated exclusively in B2 tumors (p<0.05, t-test). These findings will contribute to clarify the importance of genetic factors in CC.

Publication Title

The Amerindian mtDNA haplogroup B2 enhances the risk of HPV for cervical cancer: de-regulation of mitochondrial genes may be involved.

Sample Metadata Fields

Specimen part

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accession-icon GSE51379
transcriptional changes in sweet orange in response to infection by citrus canker bacteria and their effector proteins PthAs and PthCs
  • organism-icon Citrus sinensis
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Citrus Genome Array (citrus)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of putative TAL effector targets of the citrus canker pathogens shows functional convergence underlying disease development and defense response.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon GSE85029
Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.

Sample Metadata Fields

Specimen part

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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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