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accession-icon GSE8388
Epigenetic upregulation of B-cell inappropriate genes induces extinction of B-cell program in classical Hodgkin lymphoma
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A unique feature of the tumour cells (Hodgkin/Reed-Sternberg (HRS)) of classical Hodgkin lymphoma (cHL) is the loss of their B-cell phenotype despite their B-cell origin. Several lines of evidence suggest that epigenomic events, especially promoter DNA-methylation, are involved in this silencing of many B-cell associated genes. Here we show that DNA-demethylation alone or in conjunction with histone-acetylation is not able to reconstitute the B-cell gene expression program in cultured HRS cells. Instead, combined DNA-demethylation and histone-acetylation of B cells induce a nearly complete extinction of their B-cell expression program and a tremendous up-regulation of numerous cHL characteristic genes including key players such as Id2 known to be involved in the suppression of the B-cell phenotype. Since the up-regulation of cHL characteristic genes and the extinction of the B-cell expression program occurred simultaneously, epigenetic changes may also be responsible for the malignant transformation of cHL. The epigenetic up-regulation of cHL characteristic genes thus play - in addition to promoter DNA-hypermethylation of B-cell associated genes a pivotal role for the reprogramming of HRS cells and explain why DNA-demethylation alone is unable to reconstitute the B-cell expression program in HRS cells.

Publication Title

Histone acetylation and DNA demethylation of B cells result in a Hodgkin-like phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11809
Lung transcriptome from M. avium infected WT, IFNg-/- and IRF1-/- mice
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Mycobacterium avium infection in mice induces granuloma necrosis in the lung which is dependent on IFNg. IRF1 is a transcription factor activated by IFNg signaling. The effect of IFNg and IRF1 on immunopathology and transcriptional changes in the lung were analysed using gene-deficient mice.

Publication Title

Mycobacteria-induced granuloma necrosis depends on IRF-1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14316
Impact of IL-10 pulmonary gene expression in mouse M. tuberculosis infection
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The cytokine IL-10 deactivates macrophages and has been shown to impair resistance to mycobacterial infection. We have infected transgenic mice overexpressing IL-10 under control of the macrophage-specific CD68 promoter (macIL-10tg mice) with Mycobacterium tuberculosis by aerosol and found increased bacterial loads in the lungs of macIL-10tg mice.

Publication Title

Autocrine IL-10 induces hallmarks of alternative activation in macrophages and suppresses antituberculosis effector mechanisms without compromising T cell immunity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE61494
The glucosinolate metabolite 1-methoxy-3-indolylmethyl alcohol induces a gene expression profile in mouse liver similar to the expression signature caused by known genotoxic hepatocarcinogens
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Breakdown products of some glucosinolates defense chemicals of Brassicales induce detoxifying enzymes and demonstrate preventive activities against chemically induced tumorigenesis in animal models. However, other breakdown products are genotoxic. 1-Methoxy-3-indolylmethyl alcohol (1-MIM-OH) is mutagenic in bacterial and mammalian cells upon activation by sulphotransferases and forms DNA adducts in mouse tissues. This effect was enhanced in mice transgenic for human sulphotransferases 1A1/2 (FVB/N-hSULT1A1/2). In this study we explored gene expression changes induced by 1-MIM-OH in mouse liver. FVB/N-hSULT1A1/2 mice were orally treated with 1-MIM-OH for 21 or 90 days, leading to high levels of hepatic 1-MIM-DNA adducts. Genome-wide expression analyzes in this tissue demonstrated no influence on detoxifying enzymes, but up-regulation of many mediators of the tumour suppressor p53 and down-regulation of Fhit and other long genes. In conclusion, 1-MIM-OH did not induce protective enzymes, but formed high levels of DNA adducts, which were recognized by affected cells as reflected by p53 activation. While this p53 response might aim to protection, it was unable to prevent the accumulation of DNA adducts. However, various epdemiological studies reported inverse associations between the intake of cruciferous vegetables and cancer. This association might be due to the presence of other glucosinolates with tumour-preventing influences possibly outweighing adverse effects of some metabolites. Nevertheless, 1-MIM-OH is a genotoxic substance inducing a gene expression profile similar to the expression signature caused by known genotoxic hepatocarcinogens.

Publication Title

The glucosinolate metabolite 1-methoxy-3-indolylmethyl alcohol induces a gene expression profile in mouse liver similar to the expression signature caused by known genotoxic hepatocarcinogens.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE21254
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE21252
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation: expression of A/T-treated vs. untreated B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE21251
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation: expression of Hodgkin vs. B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE28079
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation: expression of PCM vs. B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE33627
Expression data of IL-18 generated murine NK cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We analyzed gene expression profiles of IL-18 generated murine NK cells in comparison to unstimulated, freshly isolated splenic NK cells.

Publication Title

Immunoregulatory natural killer cells suppress autoimmunity by down-regulating antigen-specific CD8+ T cells in mice.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE30726
Deep sequencing of MYC DNA-binding sites in Burkitt's lymphoma
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background: MYC is a transcription factor encoded by the c-MYC gene (thereafter termed MYC). MYC is key transcription factor involved in many central cellular processes including ribosomal biogenesis. MYC is overexpressed in the majority of human tumours including aggressive B-cell lymphoma especially Burkitt's lymphoma. Although Burkitt's lymphoma is a highlight example for MYC overexpression due to a chromosomal translocation, no global analysis of MYC binding sites by chromatin immunoprecipitation (ChIP) followed by global next generation sequencing (ChIP-Seq) has been conducted so far in Burkitt's lymphoma.

Publication Title

Deep sequencing of MYC DNA-binding sites in Burkitt lymphoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples

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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