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accession-icon GSE85942
Large-Scale Atlas of Mutant IDH1-Dependent Chromatin State Reprogramming, Reversibility, and Persistence
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Mutant-IDH1-dependent chromatin state reprogramming, reversibility, and persistence.

Sample Metadata Fields

Specimen part

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accession-icon GSE19615
Integrated genomic and function characterization of the 8q22 gain
  • organism-icon Homo sapiens
  • sample-icon 113 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Integrated DNA and expression array analysis in primary human breast tumors identified chromosome 8q22 copy number gain and a suite of over-expressed genes in this region highly relevant to subsequent recurrence.

Publication Title

Amplification of LAPTM4B and YWHAZ contributes to chemotherapy resistance and recurrence of breast cancer.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE64763
Expression data from normal myometrium, leiomyomata, and leiomyosarcomas
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The molecular etiology of uterine leiomyosarcoma (ULMS) is poorly understood, which accounts for the wide disparity in outcomes among women with this disease. We examined and compared the molecular profiles of ULMS, fibroids, and normal myometrium (NL) to identify clinically relevant molecular subtypes. RNA was hybridized to Affymetrix U133A 2.0 transcription microarrays. Differentially expressed genes and pathways were identified using standard methods.

Publication Title

Molecular subtypes of uterine leiomyosarcoma and correlation with clinical outcome.

Sample Metadata Fields

Sex

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accession-icon GSE37088
Follicular Lymphoma expression array
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We used microarrays to detail gene expression profile of several follicular lymphoma patient samples with different grades

Publication Title

Frequent disruption of the RB pathway in indolent follicular lymphoma suggests a new combination therapy.

Sample Metadata Fields

Specimen part

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accession-icon GSE24558
GBM brain tumors
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Glioblastoma stem-like cells give rise to tumour endothelium.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE51448
Gene expression analysis of estrogen receptor mutants, S463P, Y537S and D538G in MCF7 cells
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of MCF7 cells transfected with ER mutants (S463P, Y537S and D538G) in phenol-red free, charcoal stripped FBS media and regular DMEM/F12 media. Results provide insight on the gene expression profiles induced by the various ER mutants.

Publication Title

ESR1 ligand-binding domain mutations in hormone-resistant breast cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE85939
Large-Scale Atlas of Mutant IDH1-Dependent Chromatin State Reprogramming, Reversibility, and Persistence [expression microarray]
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutations drive the development of gliomas and other human malignancies. Significant efforts are already underway to attempt to target mutant IDH in clinical trials. However, how mutation of IDH leads to tumorigenesis is poorly understood. Mutant IDH1 promotes epigenetic changes that promote tumorigenesis but the scale of these changes throughout the epigenome and the reversibility of these changes are unknown. Here, using both human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant IDH1-induced epigenomic reprogramming. We characterize the changes in the histone code landscape, DNA methylome, chromatin state, and transcriptional reprogramming that occur following IDH1 mutation and characterize the kinetics and reversibility of these alterations over time. We discover coordinate changes in the localization and intensity of multiple histone marks and chromatin states throughout the genome. These alterations result in systematic chromatin states changes, which result in widespread gene expression changes involving oncogenic pathways. Specifically, mutant IDH1 drives alterations in differentiation state and establishes a CD24+ population that features enhanced self-renewal and other stem-like properties. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented molecular portraits of mutant IDH1-dependent epigenomic reprogramming at high resolution. These findings have significant implications for our understanding the mechanisms underlying mutant IDH function and for optimizing therapeutic approaches to targeting IDH mutant tumors.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE70626
TH2 cytokines promote tumor progression via regulating cathepsin secretion in tumor-associated macrophages
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Tumor-associated macrophages (TAMs) have emerged as prominent cells within the tumor microenvironment playing critical roles in extracellular matrix remodeling, tumor cell proliferation and invasion, angiogenesis, and metastasis. Cathepsin proteases, produced by tumor cells and TAMs, have been demonstrated to mediate these processes, but it still remains unclear how these typically lysosomal enzymes are capable of executing their functions in the extracellular space. Here we identify a novel interaction between STAT6 and STAT3 that potently upregulates cathepsin secretion in macrophages in response to TH2 cytokine stimulation. Systematic gene expression analyses reveal that the TH2 cytokine IL-4 synergizes with IL-6 or IL-10 to activate the IRE1/ XBP1 axis of the unfolded protein response. Pharmacological inhibition of the IRE1 axis blunts cathepsin secretion in macrophages and blocks macrophage-mediated tumor cell invasion. Finally, we show that genetic ablation of either STAT6 or STAT3 signaling impairs tumor development and invasion. Thus, these findings demonstrate that TH2 cytokine-mediated STAT6 and STAT3 activation in macrophages promotes a professional secretory phenotype capable of enhancing tumor cell invasion in a cathepsin-dependent manner.

Publication Title

No associated publication

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE14108
Brain metastasis from lung adenocarcinoma patients
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Microarray analysis of 28 brain metastasis samples from lung adenocarcinoma patients.

Publication Title

Isolated metastasis of an EGFR-L858R-mutated NSCLC of the meninges: the potential impact of CXCL12/CXCR4 axis in EGFR<sub>mut</sub> NSCLC in diagnosis, follow-up and treatment.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26459
High-throughput ectopic expression screen for tamoxifen resistance
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Resistance to tamoxifen in breast cancer patients is a serious therapeutic problem and major efforts are underway to understand underlying mechanisms. Resistance can be either intrinsic or acquired. We derived a series of subcloned MCF7 cell lines that were either highly sensitive or naturally resistant to tamoxifen and studied the factors that lead to drug resistance. Gene-expression studies revealed a signature of 67 genes that differentially respond to tamoxifen in sensitive vs. resistant subclones, which also predicts disease-free survival in tamoxifen-treated patients. High-throughput cell-based screens, in which >500 human kinases were independently ectopically expressed, identified 31 kinases that conferred drug resistance on sensitive cells. One of these, HSPB8, was also in the expression signature and, by itself, predicted poor clinical outcome in one cohort of patients. Further studies revealed that HSPB8 protected MCF7 cells from tamoxifen and blocked autophagy. Moreover, silencing HSBP8 induced autophagy and caused cell death. Tamoxifen itself induced autophagy in sensitive cells but not in resistant ones, and tamoxifen-resistant cells were sensitive to the induction of autophagy by other drugs. These results may point to an important role for autophagy in the sensitivity to tamoxifen.

Publication Title

High-throughput ectopic expression screen for tamoxifen resistance identifies an atypical kinase that blocks autophagy.

Sample Metadata Fields

Specimen part, Cell line

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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)

fund-icon Fund the CCDL

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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