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accession-icon GSE23501
DNA methylation signatures define molecular subtypes of Diffuse Large B Cell Lymphoma
  • organism-icon Homo sapiens
  • sample-icon 67 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We performed DNA methylation (HELP array) and gene expression profiling in 69 samples of diffuse large B cell lymphoma (DLBCL). First, by gene expression, two molecular subtypes of DLBCL termed as "germinal center B cell-like" (GCB) and "activated B cell-like" (ABC) DLBCL were assigned to the 69 DLBCL cases. Then, the supervised analysis using HELP data revealed strikingly different DNA promoter methylation patterns in the two molecular DLBCL subtypes. These data provide epigenetic evidence that the DLBCL subtypes are distinct diseases that utilize different oncogenic pathways.

Publication Title

DNA methylation signatures define molecular subtypes of diffuse large B-cell lymphoma.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE13401
The purine scaffold HSP90 inhibitor PU-H71 induces specific changes in gene expression in DLBCL xenografts.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Heat shock protein 90 (Hsp90) is an emerging therapeutic target in cancer. We report that Hsp90 inhibitors selectively kill DLBCLs that are biologically dependent on the BCL6 transcriptional repressor. We examined the pharmacokinetics, toxicity and efficacy of PUH71, a recently developed purine scaffold Hsp90 inhibitor. PUH71 preferentially accumulated in tumors vs. normal tissues, and unlike the widely used benzoquinone Hsp90 inhibitors, displayed no signs of organ toxicity. PUH71 selectively and potently induced the regression of BCL6-dependent DLBCLs in vivo, through reactivation of key BCL6 target genes and apoptosis.

Publication Title

A purine scaffold Hsp90 inhibitor destabilizes BCL-6 and has specific antitumor activity in BCL-6-dependent B cell lymphomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP174055
Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Lung adenocarcinoma (LUAD)-derived oncogenic Wnts increase cancer cell proliferative/stemness potential, but whether they also impact the immune microenvironment is unknown. Here we show that LUAD cells use paracrine Wnt1 signaling to induce immune resistance. Wnt1 correlated strongly with tolerogenic genes on the TCGA expression data. In another cohort, Wnt1 was inversely associated with T cell abundance. Altering Wnt1 expression profoundly affected growth of murine lung adenocarcinomas and this was strongly dependent on conventional dendritic cells and T cells. Mechanistically, Wnt1 lead to transcriptional silencing of CC/CXC chemokines in dendritic cells and T cell cross-tolerance. Wnt-target genes were up-regulated in human intratumoral dendritic cells and decreased upon silencing Wnt1, accompanied by enhanced T cell cytotoxicity. siWnt1-loaded nanoparticles as single therapy or part of combinatorial immunotherapies acted at both arms of the cancer-immune ecosystem to halt tumor growth. Collectively, our studies show that Wnt1 enhances adaptive immune rejection of lung adenocarcinomas and highlight its potential targeting as a novel therapeutic strategy  Overall design: RNAseq data of two DC subsets of 4 patients with lung adenocarcinomas (LUADs).

Publication Title

Wnt1 silences chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

View Samples
accession-icon SRP171054
Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

This study showed that the oncogenic ligand Wnt1 silences chemokine genes in dendritic cells, leading to impaired cross-priming of T cells in lung adenocarcinoma. Blocking Wnt1 enhanced rejection of tumors by acting concomitantly at the cancer and immune cell level. Overall design: 3' RNA-Seq (QuantSeq) profiling of sorted cDCs populations from WNT1 overexpressing and control (Empty) lung tumors.

Publication Title

Wnt1 silences chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE73739
Transcriptional and Behavioral Responses of Zebrafish Larvae to Microcystin-LR Exposure
  • organism-icon Danio rerio
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Zebrafish Gene 1.0 ST Array (zebgene10st)

Description

Microcystin-LR (MC-LR), the most toxic member of microcystin family, inhibits protein phosphatase PP2A, triggers oxidative stress and induces hepatotoxicity. Gene expression profiling of MC-LR treated larvae using DNA microarray analysis revealed effects in the retinal visual cycle and pigmentation synthesis pathways that have not been previously associated with MC-LR. Liver-related genes were also differentially expressed. The microarray data were confirmed by quantitative real-time PCR. Our findings provide new evidence that microcystin-LR exposure of zebrafish larvae modulates the retinal visual cycle and pigmentation synthesis pathways and ultimately alter larval zebrafish behavior

Publication Title

Transcriptional and Behavioral Responses of Zebrafish Larvae to Microcystin-LR Exposure.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP049237
MiR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction [III]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Identifying the interaction partners of non-coding RNAs is essential for elucidating their functions. We have developed an approach, termed microRNA-cross-linking and immunoprecipitation (miR-CLIP), using pre-miRNAs modified with psoralen and biotin to capture their targets in cells. Photo-cross-linking and Argonaute 2-immunopurification followed by streptavidin affinity-purification of probe-linked RNAs provided selectivity in the capture of targets, identified by deep-sequencing. MiR-CLIP with pre-miR-106a, a miR-17-5p family member, identified hundreds of putative targets in HeLa cells, many carrying conserved sequences complementary to the miRNA seed but also many that were not predicted computationally. MiR-106a overexpression experiments confirmed that miR-CLIP captured functional targets, including H19, a long-non-coding RNA that is expressed during skeletal muscle cell differentiation. We showed that miR-17-5p family members bind H19 in HeLa cells and myoblasts. During myoblast differentiation levels of H19, miR-17-5p family members and mRNA targets changed in a manner suggesting that H19 acts as a sponge for these miRNAs. Overall design: Two replicates of three cDNA libraries were submitted to deep sequencing: a sample from RNA-7-transfected cells; a sample from pre-miR-106a transfected cells; and a control sample.

Publication Title

miR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP049238
MiR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction [IV]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Identifying the interaction partners of non-coding RNAs is essential for elucidating their functions. We have developed an approach, termed microRNA-cross-linking and immunoprecipitation (miR-CLIP), using pre-miRNAs modified with psoralen and biotin to capture their targets in cells. Photo-cross-linking and Argonaute 2-immunopurification followed by streptavidin affinity-purification of probe-linked RNAs provided selectivity in the capture of targets, identified by deep-sequencing. MiR-CLIP with pre-miR-106a, a miR-17-5p family member, identified hundreds of putative targets in HeLa cells, many carrying conserved sequences complementary to the miRNA seed but also many that were not predicted computationally. MiR-106a overexpression experiments confirmed that miR-CLIP captured functional targets, including H19, a long-non-coding RNA that is expressed during skeletal muscle cell differentiation. We showed that miR-17-5p family members bind H19 in HeLa cells and myoblasts. During myoblast differentiation levels of H19, miR-17-5p family members and mRNA targets changed in a manner suggesting that H19 acts as a sponge for these miRNAs. Overall design: Two replicates of two cDNA libraries were submitted to deep sequencing: a sample from siH19-transfected cells and a control sample.

Publication Title

miR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE59865
Cell type-specific requirements for iPSC reprogramming
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The differentiated state of somatic cells provides barriers for the efficient derivation of induced pluripotent stem cells (iPSCs). To address why some cell types reprogram more readily than others, we studied the effect of combined modulation of cellular signaling pathways. This revealed that inhibition of TGF together with activation of Wnt signaling in presence of ascorbic acid allows >80% of murine fibroblasts to acquire pluripotency after one week of reprogramming factor expression. In contrast, hepatic progenitors and blood progenitors predominantly required only TGF inhibition or canonical Wnt activation, respectively, to reprogram at efficiencies approaching 100%. Strikingly, blood progenitors reactivated endogenous pluripotency loci in a highly synchronous manner. We further demonstrate that expression of specific chromatin-modifying enzymes and reduced TGF/MAP kinase activity are intrinsic properties associated with the unique reprogramming response of these cells. Together, our observations define novel cell type-specific requirements for the rapid and synchronous reprogramming of somatic cells.

Publication Title

Combinatorial modulation of signaling pathways reveals cell-type-specific requirements for highly efficient and synchronous iPSC reprogramming.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon SRP147923
Human blastocysts of normal and abnormal karyotypes display distinct transcriptome profiles: an analysis of every mono and trisomy
  • organism-icon Homo sapiens
  • sample-icon 99 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Characterization of the transcriptome of normal and abnormal embryos. Overall design: Gene expression profiling of every mono and trisomy.

Publication Title

Human blastocysts of normal and abnormal karyotypes display distinct transcriptome profiles.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE11722
Irinotecan-induced gene expression changes in the rat intestine
  • organism-icon Rattus norvegicus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The regional specificity and timing of gene activation following chemotherapy, and how this relates to subsequent mucositis development is currently unknown. The aim of the study was therefore to determine the early time course of gene expression changes along the gastrointestinal tract (GIT) of the DA rat following irinotecan treatment, so as to provide an insight into the genetic component of mucositis.

Publication Title

Gene expression analysis of multiple gastrointestinal regions reveals activation of common cell regulatory pathways following cytotoxic chemotherapy.

Sample Metadata Fields

Sex, Age

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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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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