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accession-icon GSE22522
Comparison of the transcriptome of K-LEC spheroids to control LEC spheroids
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions.The disease is caused by the KSHV virus (HHV8) and is recognisable by its distinctive red skin lesions. The lesions are KSHV infected spindle cells expressing markers of the lymphatic endothelial and blood vessel endothelial cells as well as other cell types. The effects of KSHV infection of lymphatic endothelial cells (LEC) cultured in 3D matrix for three days were assayed using Affymetrix hgu133plus2 chips.

Publication Title

KSHV-initiated notch activation leads to membrane-type-1 matrix metalloproteinase-dependent lymphatic endothelial-to-mesenchymal transition.

Sample Metadata Fields

Specimen part

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accession-icon GSE41856
Cell growth in aggregates determines gene expression, proliferation, survival and chemoresistance of Follicular Lymphoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cell growth in aggregates determines gene expression, proliferation, survival, chemoresistance, and sensitivity to immune effectors in follicular lymphoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41855
Expression data from quiescent cells and cycling cells isolated from Multicellular aggregates of lymphoma cells (MALC)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Follicular Lymphomas are blood tumors growing as spheres in patients. Before this study, there was no experimental model mimicking the 3D organization of these in vivo tumors. We develop such a model, called MALC, and observed a progressive enrichment in quiescent cells in these with time of culture; these cells were sorted, as their cycling counterparts, and their transcriptomes were compared. We used microarrays to detail the differential global gene expression profile between quiescent and cycling cells isolated from MALC.

Publication Title

Cell growth in aggregates determines gene expression, proliferation, survival, chemoresistance, and sensitivity to immune effectors in follicular lymphoma.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE41851
Expression data from follicular lymphoma cells cultured either in suspension either as Multicellular aggregates of lymphoma cells (MALC)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Follicular Lymphomas are blood tumors growing as spheres in patients. Before this study, there was no experimental model mimicking the 3D organization of these in vivo tumors. We develop such a model, called MALC, and performed a pan-genomic comparative analysis between MALC and classical suspension cultures. We used microarrays to detail the global gene expression profile induced by aggregated growth of lymphoma cells.

Publication Title

Cell growth in aggregates determines gene expression, proliferation, survival, chemoresistance, and sensitivity to immune effectors in follicular lymphoma.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE84072
Expression data from CD8+TIM-3+ and CD8+TIM-3- T cells sorted from follicular lymphoma lymph nodes
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Exhaustion markers are expressed by T lymphocytes in Follicular Lymphoma (FL). Through these, TIM-3 has been recently identified as a poor pronostic factor when expressed by FL CD4+ T cells.

Publication Title

Impaired functional responses in follicular lymphoma CD8<sup>+</sup>TIM-3<sup>+</sup> T lymphocytes following TCR engagement.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE29305
NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

View Samples
accession-icon GSE29148
NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming.

Publication Title

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

View Samples
accession-icon GSE29147
NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming.

Publication Title

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

View Samples
accession-icon GSE19556
Transcriptional program of terminal granulocytic differentation
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

To characterize the transcriptional program that governs terminal granulocytic differentation in vivo, we performed comprehensive microarray analysis of human bone marrow population highly enriched for promyelocytes, myelocytes / metamyelocytes and neotrophils.

Publication Title

Human neutrophils secrete bioactive paucimannosidic proteins from azurophilic granules into pathogen-infected sputum.

Sample Metadata Fields

Specimen part

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accession-icon GSE31280
Transcript level in F9 teratocarcinoma WT and RARalpha knockout in presence and absence of all-trans retinoic acid
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Retinoic acid receptors (RARs) , and are key regulators of embryonic development. Hematopoietic differentiation is regulated by RAR, and several types of leukemia show aberrant RAR activity. We demonstrate that RAR plays an important role in cellular memory and imprinting by regulating the CpG methylation status of specific promoter regions.

Publication Title

Epigenetic regulation by RARα maintains ligand-independent transcriptional activity.

Sample Metadata Fields

Cell line, Treatment

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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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