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accession-icon GSE11357
Irradiated stroma selects for invasive and metastatic tumoc cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Radiotherapy is widely used to treat human cancer. Patients locally recurring after radiotherapy, however, have increased risk of metastatic progression and poor prognosis. The clinical management of post-radiation recurrences remains an unresolved issue. Tumors growing in pre-irradiated tissues have an increased fraction of hypoxic cells and are more metastatic, a condition known as tumor bed effect. Here we demonstrate that tumor cells growing in a pre-irradiated bed, or selected in vitro though repeated cycles of severe hypoxia, retain an invasive and metastatic capacities when returned to normoxia. HIF activity, while it facilitates metastatic spreading of tumors growing in a pre-irradiated bed, is not essential. Through gene expression profiling and gain and loss of function experiments, we identified the matricellular protein CYR61 and aVb5 integrin, as proteins cooperating to mediate these effects. Inhibition of aVb5 integrin suppressed invasion and metastasis induced by CYR61 and attenuated metastasis of tumors growing within a pre-irradiated field. These results represent a conceptual advance to the understanding of the tumor bed effect and identify CYR61 and aVb5 integrin as proteins that co-operate to mediate metastasis. They also indicate aV integrin inhibition a potential therapeutic approach for preventing metastasis in patients at risk for post-radiation recurrences, which can be promptly tested in the clinic.

Publication Title

CYR61 and alphaVbeta5 integrin cooperate to promote invasion and metastasis of tumors growing in preirradiated stroma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE95613
Expression data from Drosophila tumor models
  • organism-icon Drosophila melanogaster
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.0 ST Array (drogene10st)

Description

Epithelial tumors can progress from a benign tissue overgrowth (hyperplasia) to a malignant neoplastic tumor, which is characterized by an increase in motility and invasiveness. The Cohen laboratory has developed an epithelial tumor model in which overexpression of the epidermal growth factor receptor gene (EGFR) leads to benign tissue hyperplasia. When combined with other cooperating factors, EGFR overexpression can lead to neoplasia and malignant metastasis.

Publication Title

Warburg Effect Metabolism Drives Neoplasia in a Drosophila Genetic Model of Epithelial Cancer.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE76002
Maternal Obesity is Associated with Ovarian Inflammation and Up-regulation of Early Growth Response Factor (Egr)-1
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Maternal obesity during the pre-implantation period leads to a pro-inflammatory milieu in the ovaries. We conducted a global transcriptomic profiling in ovaries from TEN fed rats during the pre-implantation period. Microarray analysis revealed that obesity lead to increased expression of genes related to inflammation, decreased glucose transporters, and dysregulation of ovarian function-related genes in the ovaries. Our results suggest maternal obesity led to an up-regulation of inflammatory genes and Egr-1 protien expression in peri-implantation ovarian tissue, and a concurrent down-regulation of glucose transporters mRNA and AKT and PI3K protein levels.

Publication Title

Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP136315
Th1 and T17 activation with and without CB839 treatment
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 3000

Description

Activated T cells differentiate into functional subsets which require distinct metabolic programs. Glutaminase (GLS) converts glutamine to glutamate to provide substrate for the tricarboxylic acid cycle and epigenetic reactions and here we identify a key role for GLS in T cell activation and specification. Though GLS-deficiency diminished T cell activation, proliferation and impaired differentiation of Th17 cells, loss of GLS also increased Tbet and Interferon-? expression and CD4 Th1 and CD8 CTL effector cell differentiation. These changes were mediated by differentially altered gene expression and chromatin accessibility, leading to increased sensitivity of Th1 cells to IL-2 mediated mTORC1 signaling. In vivo, GLS-null T cells failed to drive a Th17-mediated Graft-vs-Host Disease model. Transient inhibition of GLS, however, increased Th1 and CTL T cell numbers in viral and chimeric antigen receptor models. Glutamine metabolism thus has distinct roles to promote Th17 but constrain Th1 and CTL effector cell differentiation. Overall design: Cells were treated with glutaminase1 inhibitor or vehicle

Publication Title

Distinct Regulation of Th17 and Th1 Cell Differentiation by Glutaminase-Dependent Metabolism.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE139401
Genome-wide analysis of gene expression response to type II ribosome inactivating protein stenodactylin
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Time-series analysis of response to ribosome 28s damage at gene expression level

Publication Title

Early Response to the Plant Toxin Stenodactylin in Acute Myeloid Leukemia Cells Involves Inflammatory and Apoptotic Signaling.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE27583
mRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs.

Publication Title

CUGBP1 and MBNL1 preferentially bind to 3' UTRs and facilitate mRNA decay.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE43685
Early growth response protein-1 coordinates lipotoxicity-associated placental inflammation: Role in Maternal Obesity
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Maternal obesity during pregnancy leads to a pro-inflammatory milieu in the placenta. We conducted a global transcriptomic profiling in BeWo cells following palmitic acid (PA, 500 uM) and/or TNF-alpha (10 ng/ml) treatment for 24 h. Microarray analysis revealed that placental cytotrophoblasts increased expression of genes related to inflammation, stress response and immediate-early factors in response to plamitic acid, TNF-alpha or a combination of both. Our results suggest that fatty acids and inflammatory cytokines induce inflammation in placental cells via activation of JNK-Egr-1 signaling.

Publication Title

Early growth response protein-1 mediates lipotoxicity-associated placental inflammation: role in maternal obesity.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29420
Expression data of pmr1 mutants
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The yeast PMR1 (ATP2C1) gene codes for the eukaryotic prototype of a high affinity P-type ATPase required for Ca2+/Mn2+ transport into the Golgi. Cells lacking PMR1 exhibit multiple genetic interactions with genes involved in DNA recombination and replication, a fact that is not yet understood. We find that deletion of PMR1 causes a delay in DNA replication initiation, progression and G2/M transition and induces the transcriptional up-regulation of genes involved in cell cycle regulation, including CLB5 and SWE1. Interestingly, pmr1 clb5 double mutants exhibit a dramatic delay in DNA replication and increased DNA breakage, while endoreplication and the formation of multi-nucleated, giant yeast is observed in pmr1 swe1 cells. Because these phenotypes can be attributed to impeded Mn2+-pump function, we provide a model in which Mn2+ interferes with Mg2+ in the nucleus, and vice versa, Mg2+ interferes with Mn2+ in the Golgi. Consequently, cell cycle progression is challenged by aberrant catalytic activities of enzymes involved in replication and protein glycosylation.

Publication Title

Impaired manganese metabolism causes mitotic misregulation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE100326
Effect of developmental NMDAR antagonism on aspartame-induced hypothalamic and adrenal gene expression
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE100324
Expression data from adult mouse adrenal tissue
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Chronic dietary aspartame may impair rodent insulin tolerance and may affect behavior. Previous studies have shown the aspartame effects may be modulated by developmental NMDA receptor antagonism. Present study was designed to assess effects of aspartame and NMDAR antagonism on components of the HPA axis.

Publication Title

Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
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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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