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accession-icon GSE59459
Identification of megakaryoblastic leukemia-1 (Mkl1) target genes in 4T1 mammary carcinoma cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The present study was designed to identify Mkl1 target genes whose expression requires either the B1 site of Mkl1 and serum response factor (SRF), respectively, or the SAP domain of Mkl1. For this purpose, we obtained the transcriptomes of four stable 4T1 cell lines that either overexpress full length Mkl1-RFP (4T1-FL), Mkl1-RFP with a mutated SRF-interaction site (4T1-mutB1), Mkl1-RFP with a deletion of the SAP domain (4T1-SAP) or an empty vector encoding RFP alone (4T1 control).

Publication Title

Mechanism of irradiation-induced mammary cancer metastasis: A role for SAP-dependent Mkl1 signaling.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE64193
Transcript profiling of mouse 4T1 tumors grown in preirradiated vs. nonirradiated mammary tissue
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The present study was designed to identify genes induced by irradiation in the 4T1 breast cancer model mimicking aggressive local relapse after radiotherapy. For this purpose, we obtained the transcriptomes of 4T1 tumors grown in either preirradiated (IRR+4T1) or non-irradiated (4T1) mammary tissue.

Publication Title

Mechanism of irradiation-induced mammary cancer metastasis: A role for SAP-dependent Mkl1 signaling.

Sample Metadata Fields

Specimen part

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accession-icon GSE22813
Transcriptome of the bone metastasis associated stroma
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The reciprocal interaction between cancer cells and the tissue-specific stroma is critical for primary and metastatic tumor growth progression. Prostate cancer cells colonize preferentially bone (osteotropism), where they alter the physiological balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption, and elicit prevalently an osteoblastic response (osteoinduction). The molecular cues provided by osteoblasts for the survival and growth of bone metastatic prostate cancer cells are largely unknown. We exploited the sufficient divergence between human and mouse RNA sequences together with redefinition of highly species-specific gene arrays by computer-aided and experimental exclusion of cross-hybridizing oligonucleotide probes. This strategy allowed the dissection of the stroma (mouse) from the cancer cell (human) transcriptome in bone metastasis xenograft models of human osteoinductive prostate cancer cells (VCaP and C4-2B). As a result, we generated the osteoblastic bone metastasis-associated stroma transcriptome (OB-BMST). Subtraction of genes shared by inflammation, wound healing and desmoplastic responses, and by the tissue type-independent stroma responses to a variety of non-osteotropic and osteotropic primary cancers generated a curated gene signature (Core OB-BMST) putatively representing the bone marrow/bone-specific stroma response to prostate cancer-induced, osteoblastic bone metastasis. The expression pattern of three representative Core OB-BMST genes (PTN, EPHA3 and FSCN1) seems to confirm the bone specificity of this response. A robust induction of genes involved in osteogenesis and angiogenesis dominates both the OB-BMST and Core OB-BMST. This translates in an amplification of hematopoietic and, remarkably, prostate epithelial stem cell niche components that may function as a self-reinforcing bone metastatic niche providing a growth support specific for osteoinductive prostate cancer cells. The induction of this combinatorial stem cell niche is a novel mechanism that may also explain cancer cell osteotropism and local interference with hematopoiesis (myelophthisis). Accordingly, these stem cell niche components may represent innovative therapeutic targets and/or serum biomarkers in osteoblastic bone metastasis.

Publication Title

The molecular signature of the stroma response in prostate cancer-induced osteoblastic bone metastasis highlights expansion of hematopoietic and prostate epithelial stem cell niches.

Sample Metadata Fields

Specimen part

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accession-icon GSE110023
Glatiramer Acetate modulates ion channel expression and calcium homeostasis in B-cell of patients with relapsing-remitting multiple sclerosis
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In order to investigate the effects of Glatiramer acetate (GA) in treatment-nave RR-MS female patients B cells we performed Affymetrix Gene-Chip Human Genome HG-U133A_2 hybridization experiments

Publication Title

Glatiramer Acetate modulates ion channels expression and calcium homeostasis in B cell of patients with relapsing-remitting multiple sclerosis.

Sample Metadata Fields

Sex, Specimen part, Disease, Subject

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accession-icon SRP060444
RNA-seq analyses of kdm5 mutant flies and wt flies under normal condition and oxidative stress
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Comparing the transcriptome of wildtype and kdm5 mutant flies in normal conditions revealed a total of 4787 genes that were significantly downregulated and thus require KDM5 for their activation, and 3269 upregulated genes that are normally repressed by KDM5 (p<0.05, FDR <0.05). Because kdm5 mutants are sensitive to the oxidizer paraquat, we also carried out RNA-seq from wildtype and kdm5 mutant adults in oxidative stress conditions. Paraquat treatment of wildtype flies lead to the upregulation of 2481, and downregulation of 3103 genes Overall design: adult mRNA profiles of 1-3-days old wild type (WT) and kdm5 mutant under normal condition and oxitative stress were generated by deep sequencing, using Illumina HisSeq 2000.

Publication Title

The Histone Demethylase KDM5 Activates Gene Expression by Recognizing Chromatin Context through Its PHD Reader Motif.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE24118
Secreted Factors from Staphylococcus aureus Biofilm and Planktonic Cultures Differentially Impact Human Keratinocytes, in vitro
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Interactions between human keratinocytes and secreted factors from Staphylococcus aureus biofilm and planktonic cultures were investigated using microarray analysis.

Publication Title

Staphylococcus aureus Biofilm and Planktonic cultures differentially impact gene expression, mapk phosphorylation, and cytokine production in human keratinocytes.

Sample Metadata Fields

Treatment

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accession-icon SRP110626
RNA-seq analyses of kdm5[A512P] and enzymatically inactive kdm5[JmjC*] in adult heads
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study was to generate a Drosophila model of intellectual disability caused by mutations in kdm5. RNA-seq was used to define the transcriptional defects of a mutation in Drosophila that is analogous to a human intellectual disability-associated allele, kdm5[A512p]. These data revealed a total of 1609 dysregulated genes, 778 of which were upregulated and 831 were downregulated. To determine whether these transcriptional defects were due to the loss of KDM5-induced histone demethylation, we also carried out RNA-seq from a enzymatic inactive strain, kdm5[Jmjc*]. These data revealed a striking similarity between the two datasets and suggest that the primary defect of KDM5[A512P] is loss of histone demethylase activity. Overall design: 3-5 day old adult heads from wildtype, kdm5[A512P] and kdm5[JmjC*] were used to generate RNA that was subsequently subjected to deep sequencing.

Publication Title

A Drosophila Model of Intellectual Disability Caused by Mutations in the Histone Demethylase KDM5.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE37180
Gene expression profiles of ovarian tumor biopsies from Phase I dasatinib trial
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

A phase I trial of a SRC kinase Inhibitor, dasatinib, in combination with paclitaxel and carboplatin in patients with advanced or recurrent ovarian cancer. Background: We conducted a phase I study of dasatinib, an oral SRC tyrosine kinase inhibitor, in combination with paclitaxel and carboplatin in advanced and recurrent epithelial ovarian cancer (EOC). Methods: The primary objective was to determine the maximum tolerated dose (MTD). Secondary objectives included toxicity, response rate (RR), pharmacokinetics and pharmacodynamics. Based on the 3+3 design, cohorts of 3-6 pts received paclitaxel 175 mg/m2 and carboplatin AUC 6 every three weeks with escalating doses of dasatinib (100, 120, 150 mg daily), followed by an 8 patient expansion cohort. Results: Twenty patients were enrolled between 06/07 and 12/09. The median age was 61 yrs (42-82) with a median of 2 prior regimens (0-6), and 71% had platinum-sensitive disease. There were 3-6 pts in each cohort, and 8 in the expansion cohort. Pharmacokinetics were observed over the first 2 cycles of therapy. One DLT was observed in the 100 mg dasatinib cohort (grade 3 myalgia. Other toxicities in all cycles included neutropenia (95% grade 3-4), thrombocytopenia (35% grade 3-4), and fatigue (10% grade 3). The RR was 45% (complete responses, 3/18(17%); partial responses, 5/18(28%)) and 56% (10/18) had stable disease. The PFS6-month actuarial estimate was 86%. The median PFS and OS were 7.8 and 16.2 months, respectively. Conclusions: Due to the high incidence of myelosuppression with subsequent cycles the recommended phase II dose is 150 mg daily of dasatinib in combination with paclitaxel and carboplatin. The combination was safe with evidence of clinical activity in advanced EOC.

Publication Title

A phase I trial of dasatinib, an SRC-family kinase inhibitor, in combination with paclitaxel and carboplatin in patients with advanced or recurrent ovarian cancer.

Sample Metadata Fields

Subject

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accession-icon GSE32920
Phevalin (aureusimine B) production by Staphylococcus aureus biofilm and impacts on human keratinocyte gene expression
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Staphylococcus aureus produces the cyclic dipeptides tyrvalin and phevalin (aureusimine A and B, respectively).

Publication Title

Phevalin (aureusimine B) production by Staphylococcus aureus biofilm and impacts on human keratinocyte gene expression.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP078318
Embryonic retinal development
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Embryonic retinal development Overall design: Mouse retinas at different embryonic developmental stages were isolated and mRNA expression was determined by RNA sequencing

Publication Title

Programmed mitophagy is essential for the glycolytic switch during cell differentiation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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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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