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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.

Alternate Accession IDs

E-GEOD-41856

Sample Metadata Fields

No sample metadata fields

View Samples
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.

Alternate Accession IDs

E-GEOD-41855

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.

Alternate Accession IDs

E-GEOD-41851

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.

Alternate Accession IDs

E-GEOD-84072

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP113797
Control of maize vegetative and reproductive development, fertility and rRNAs silencing by HISTONE DEACETYLASE 108 [PMeA and MiA]
  • organism-icon Zea mays
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Histone deacetylases (HDACs) catalyze the removal of acetyl groups from acetylated histone tails that consequently interact more closely with DNA, leading to chromatin state refractory to transcription. Zea mays HDA108 belongs to the Rpd3/HDA1 HDAC family and is ubiquitously expressed during development. The newly isolated hda108/hda108 insertional mutant exhibited many developmental defects: significant reduction in plant height, alterations of shoot and leaf development, alterations of inflorescence patterning and fertility. Western blot analyses and immunolocalization experiments revealed an evident increase in histone acetylation, accompanied by a marked reduction in H3K9 dimethylation, in mutant nuclei. The DNA methylation status, in the CHG sequence context, and the transcript level of ribosomal sequences were also affected in hda108 mutants, while enrichment in H3 and H4 acetylation characterizes both repetitive and non-repetitive transcriptional up-regulated loci. RNA-Seq both of young leaf and anthers indicated that transcription factor expression is highly affected and that the pollen developmental programme results as disrupted in hda108 mutants. Crosses between hda108/hda108 and epiregulator mutants did not produce any double mutant progeny indicating possible genetic interactions of HDA108 with distinct epigenetic pathways. Our findings indicate that HDA108 is directly involved in regulation of maize development, fertility and epigenetic regulation of genome activity. Overall design: Total RNA-Seq analysis of maize anthers at post-meiotic (PMeA) and mitotic (MiA) stages. 2 biological replicates for stage, each obtained by pooling anthers from three tassels per genotype were collected from wild-type and hda108 mutant plants. Strand-specific sequencing on a Illumina HiSeq2500

Publication Title

Control of Maize Vegetative and Reproductive Development, Fertility, and rRNAs Silencing by <i>HISTONE DEACETYLASE 108</i>.

Alternate Accession IDs

GSE102036

Sample Metadata Fields

Specimen part, Subject

View Samples
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.

Alternate Accession IDs

E-GEOD-31280

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE64919
Genes regulated in EML1 cells expressing the TEL-AML1 oncogene after 5 and 7 days of treatment with IL7 and FLT3 ligand.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

The t(12;21) translocation is the most common genetic rearrangement in childhood acute lymphoblastic leukemia (ALL) and gives rise to the TEL-AML1 fusion gene, which functions as a transcription factor.

Publication Title

The TEL-AML1 fusion protein of acute lymphoblastic leukemia modulates IRF3 activity during early B-cell differentiation.

Alternate Accession IDs

E-GEOD-64919

Sample Metadata Fields

Cell line, Treatment

View Samples
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.

Alternate Accession IDs

E-GEOD-29305

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.

Alternate Accession IDs

E-GEOD-29148

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.

Alternate Accession IDs

E-GEOD-29147

Sample Metadata Fields

Sex, Age, 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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