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accession-icon SRP015918
Influence of p38 MAPK (PMK-1) on the heat stress response of C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

PMK-1 is involved in the heat stress response of C. elegans, translocates to the nucleus upon heat exposure and influences the expression of chaperone genes, proteasomal subunits and protein-biosynthesis related genes. Overall design: Differential Gene expression of WT and pmk-1 deletion mutant (KU25) after 5 hours at 35°C

Publication Title

The p38 MAPK PMK-1 shows heat-induced nuclear translocation, supports chaperone expression, and affects the heat tolerance of Caenorhabditis elegans.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE24369
Gene expression profiling of low-grade fibromyxoid sarcoma (LGFMS)
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Analysis of gene expression in 17 low-grade fibromyxoid sarcoma (LGFMS) samples compared to that of histologically similar tumors. LGFMS is characterized by the specific translocations t(7;16)(q33;p11) or t(11;16)(p11;p11) and corresponding fusion genes FUS-CREB3L2 or FUS-CREB3L1.

Publication Title

FUS-CREB3L2/L1-positive sarcomas show a specific gene expression profile with upregulation of CD24 and FOXL1.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE38104
Retained heterodisomy is associated with high gene expression in hyperhaploid inflammatory leiomyosarcoma
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Retained heterodisomy is associated with high gene expression in hyperhaploid inflammatory leiomyosarcoma.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon GSE37992
Retained heterodisomy is associated with high gene expression in hyperhaploid inflammatory leiomyosarcoma (Expression)
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Global gene expression analysis of inflammatory leiomyosarcoma (ILMS) and conventional leiomyosarcoma (LMS).

Publication Title

Retained heterodisomy is associated with high gene expression in hyperhaploid inflammatory leiomyosarcoma.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP067012
Transcription profiling of neuronal metabolic reprogramming
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

we explored the changes in metabolic gene expression during neuronal differentiation from neural progenitor cells (NPC). Overall design: Examination of transcription profile in NPC and neurons.

Publication Title

Metabolic reprogramming during neuronal differentiation from aerobic glycolysis to neuronal oxidative phosphorylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE46819
Inhibitor of apoptosis protein antagonist BV6 potential for new combinatorial treatment strategies in acute myeloid leukemia
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Apoptosis is deregulated in most, if not all, cancers, including hematological malignancies. In this study, we wanted to test whether primary acute myeloid leukemia (AML) samples are sensitive for inhibitor of apoptosis (IAP) protein antagonist treatment in vitro, and which AML subgroup might profit most from such a novel therapeutic strategy. We treated diagnostic samples of 67 adult AML patients with either cytarabine (ara-C) or IAP antagonist BV6 and correlated sensitivity with clinical, cytogenetic and molecular markers, and expression levels of selected genes involved in apoptosis. Primary AML samples showed differential sensitivity to treatment with either ara-C (40% sensitive, 17% intermediate, 43% resistant) or BV6 (51% sensitive, 21% intermediate, 28% resistant). Notably, 69% of ara-C resistant samples showed a good to fair response to IAP inhibition. Furthermore, combination treatment of ara-C with BV6 showed additive effects in most samples. Differences in sensitivity to IAP antagonist treatment correlated with significantly elevated expression levels of TNF and lower levels of XIAP in BV6 sensitive samples, as well as with NPM1 mutations. Gene expression profiling pointed to apoptosis-related pathways, which were specifically induced by IAP inhibition in sensitive samples. Thus, our results suggest IAP inhibition as a potential novel therapeutic option in AML.

Publication Title

Targeting inhibitor of apoptosis proteins by Smac mimetic elicits cell death in poor prognostic subgroups of chronic lymphocytic leukemia.

Sample Metadata Fields

Sex, Age, Treatment

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accession-icon GSE62533
Inhibitor of apoptosis proteins as promising therapeutic targets in chronic lymphocytic leukemia
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Inhibitor of apoptosis (IAP) proteins are expressed at high levels in CLL cells and may contribute to evasion of cell death leading to poor therapeutic outcome. Of note, prognostic unfavourable cases with e.g. non-mutated VH-status and TP53 mutation responded significantly better to BV6 than samples with unknown or favourable prognosis e.g. 13q deletion. The majority of cases with 17p deletion (10/12) and Fludarabine refractory cases were sensitive to BV6, indicating that BV6 acts independently of the p53 pathway. Importantly, BV6 dose-dependently induced cell death in 28 of 51 (54%) investigated patient samples while B cells from healthy donors were largely unaffected. BV6 also triggered cell death under survival conditions mimicking the microenvironment e.g. by adding CD40 ligand or in conditioned medium. Gene expression profiling identified cell death- and NF-kB-signaling among the top pathways regulated by BV6. This was confirmed by data showing that BV6 causes degradation of cIAP1 and cIAP2 and NF-kB pathway activation. BV6 induced cell death depended on production of reactive oxygen species, since addition of ROS scavengers significantly rescued BV6-triggerd cell death. In contrast, BV6 induced cell death independently of caspase activity, RIP1 activity or TNF-alpha, since zVAD.fmk, necrostatin-1 or TNF-alpha-blocking antibody Enbrel failed to protect against cell death. Of note, transcripts of ROS regulatory proteins were modulated by BV6. Thus, these data have important implications for developing new therapeutic strategies to overcome cell death resistance in CLL especially in poor prognostic subgroups.

Publication Title

Targeting inhibitor of apoptosis proteins by Smac mimetic elicits cell death in poor prognostic subgroups of chronic lymphocytic leukemia.

Sample Metadata Fields

Sex, Age, Treatment

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accession-icon SRP049028
Human serotonergic neurons
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Generating human serotonergic neurons from fibroblasts

Publication Title

Generation of functional human serotonergic neurons from fibroblasts.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE67642
Expression and methylation array analysis of CD19+ B-cells from Chronic lymhocytic leukemia (CLL) patients and age matched healthy donor samples
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Krüppel-like factor 4 (KLF4) inactivation in chronic lymphocytic leukemia correlates with promoter DNA-methylation and can be reversed by inhibition of NOTCH signaling.

Sample Metadata Fields

Sex

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accession-icon GSE67640
Expression and methylation array analysis of CD19+ B-cells from Chronic lymhocytic leukemia (CLL) patients and age matched healthy donor samples [Expression]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Whole genome sequencing revealed CLL as a disease of the genome and epigenome defined by somatic mutations and aberrant DNA-methylation. To uncover the impact of aberrant methylation on transcription, gene expression and methylation array profiling was performed in CLL and B-cells. RNA from 13 CLL patients and 6 healthy donor samples was analyzed on expression arrays.

Publication Title

Krüppel-like factor 4 (KLF4) inactivation in chronic lymphocytic leukemia correlates with promoter DNA-methylation and can be reversed by inhibition of NOTCH signaling.

Sample Metadata Fields

Sex

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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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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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