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Platform
GSE87879
Homo sapiens
6 Downloadable Samples
Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
CDk4/6 inhibitor activates RB and represses RB/E2F target genes
Publication Title
RB Loss Promotes Prostate Cancer Metastasis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
CDk4/6 inhibitor activates RB and represses RB/E2F target genes
Publication Title
RB Loss Promotes Prostate Cancer Metastasis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Saccharomyces cerevisiae
- 2 Downloadable Samples
- Affymetrix Yeast Genome S98 Array (ygs98)
Description
Background
Publication Title
Global transcriptional response of Saccharomyces cerevisiae to the deletion of SDH3.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Ovarian cancer is one of the most deadly cancers accounting for only 3% of diagnosed cancers, but is the fifth leading cause of cancer deaths among woman; however, the progression of ovarian cancer is poorly understood. To study and further understand the early events that lead to epithelial derived ovarian cancer, we previously developed a cell model of progressive ovarian cancer. Mouse ovarian surface epithelial (MOSE) cells have undergone spontaneous transformation in cell culture and represent pre-neoplastic, non-tumorigenic to an aggressive malignant phenotype.
Publication Title
Changes in gene expression and cellular architecture in an ovarian cancer progression model.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We found that the non-essential amino acid L-Proline (L-Pro) acts as a signaling molecule that promotes the conversion of embryonic stem cells (ESCs) into mesenchymal-like, spindle-shaped, highly motile, invasive pluripotent stem cells. This embryonic stem cell-to-mesenchymal-like transition (esMT) is accompanied by a genome-wide remodeling of the transcriptome
Publication Title
L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 7 Downloadable Samples
Illumina HiSeq 2000
Description
Solid cancers develop within a supportive microenvironment that promotes tumor formation and continued growth through the elaboration of mitogens and chemokines. Within these tumors, monocytes (macrophages and microglia) represent rich sources of these stromal factors. Leveraging a genetically-engineered mouse model of neurofibromatosis type 1 (NF1) low-grade brain tumor (optic glioma), previous studies have demonstrated that microglia are important for glioma formation and maintenance. To identify the tumor-associated microglial factors that support glioma growth (gliomagens), we employed a comprehensive large scale discovery effort using optimized advanced RNA-sequencing methods. Candidate gliomagens were prioritized to identify potential secreted or membrane-bound proteins, which were next validated by quantitative RT-PCR and RNA FISH following minocycline-mediated microglial inactivation in vivo. Using these selection criteria, Ccl5 was identified as a highly expressed chemokine in both genetically engineered Nf1 mouse and human optic gliomas. As a candidate gliomagen, recombinant Ccl5 increased Nf1-deficient optic nerve astrocyte growth in vitro. Importantly, consistent with its critical role in maintaining tumor growth, Ccl5 inhibition with neutralizing antibodies reduced Nf1 mouse optic glioma growth in vivo. Collectively, these findings establish Ccl5 as critical stromal growth factor in low-grade glioma maintenance relevant to future microglia-targeted therapies for brain tumors. Overall design: Nf1 optic glioma associated microglia from mice were flow sorted. Upregulated genes of glioma associated microglia were verified and further examined.
Publication Title
RNA Sequencing of Tumor-Associated Microglia Reveals Ccl5 as a Stromal Chemokine Critical for Neurofibromatosis-1 Glioma Growth.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. Overall design: RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells isolated from two untreated and two 3-day Dox-treated mice.
Publication Title
Activated Notch counteracts Ikaros tumor suppression in mouse and human T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. Overall design: RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL65) cells isolated from three untreated and three 3-day Dox-treated mice. There were two sequencing runs of each RNA sample.
Publication Title
Activated Notch counteracts Ikaros tumor suppression in mouse and human T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Notch pathway activation targets AML-initiating cell homeostasis and differentiation.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Expression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation.
Publication Title
Notch pathway activation targets AML-initiating cell homeostasis and differentiation.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples