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accession-icon GSE29590
Expression data from highly purified MMTV-Neu Tumor Initiating Cells (TICs) and the non-TIC CD24- fraction
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The cancer stem cell model maintains that tumors are organized in a hierarchy driven by tumor initiating cells (TICs), and that patient survival inversely correlates with TIC gene expression. Here we generated a prognostic signature for HER2+ breast cancer from TICs purified from MMTV-Her2/Neu mammary tumors. TICs from this model, identified as Lin-:CD24+:JAG1- at a frequency of 2-5% by serial and single cell transplantation assays, showed elevated expression of proliferation genes and low expression of differentiation genes (compared to non-TIC fraction CD24- of the same tumor).

Publication Title

Seventeen-gene signature from enriched Her2/Neu mammary tumor-initiating cells predicts clinical outcome for human HER2+:ERα- breast cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE39955
Expression data comparing Pten-, p53-, and combined deficient mouse mammary tumors
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To model the effect of Pten loss on breast cancer, we deleted Pten using a floxed allele and the deleter lines MMTV-Cre(NLST), which targets stem/bi-potent progenitor cells, and WAP-Cre, which targets CD24-positive, pregnancy-identified stem cells/alveolar progenitors. Mammary tumors were detected in WAP-Cre:Ptenf/f females with a latency of 15.2 months. By 18 months, nearly all mice had succumbed to cancer. MMTV-Cre:Ptenf/f mice developed mammary tumors after a longer latency of 26.4 months and reduced penetrance (70%) compared to WAP-Cre:Ptenf/f mice. Tumors from both models were heterogeneous, consisting primarily of differentiated adenocarcinoma (adenomyoepithelioma; ~70%) and adenosquamous carcinoma (20-25%). In addition, a small fraction of tumors was classified as acinar and poorly differentiated adenocarcinoma (4-7%) and adenosarcoma (3-4%). To test the consequences of combined Pten and p53 gene mutation on breast cancer, we deleted both genes via MMTV-Cre or WAP-Cre. Kaplan-Meier tumor free survival curves revealed that WAP-Cre:Ptenf/f:p53f/f and MMTV-Cre:Ptenf/f:p53f/f females developed tumors with reduced latency of 11.3 and 9.8 months, compared with 15.2, 26.4, and 16.9 months for single-mutant WAP-Cre:Ptenf/f, MMTV-Cre:Ptenf/f or MMTV-Cre:p53f/f mice, respectively. In contrast to the heterogeneity of Pten tumors and small percentage of adenosarcomas in these mice, ~70% of Pten:p53 lesions were histologically classified as adeno-sacrcomatoid-like or mesenchymal-like breast cancer, with the rest exhibiting mixed mesenchymal plus adenocarcinomas and differentiated adenocarcinomas. The adeno-sacrcomatoid-like tumors expressed the mesenchymal markers vimentin, K5, SMA, N-cadherin and desmin but not ER, as well as islands of luminal-like K18 expressing cells surrounded by a layer of K14-positive cells.

Publication Title

Combined deletion of Pten and p53 in mammary epithelium accelerates triple-negative breast cancer with dependency on eEF2K.

Sample Metadata Fields

Specimen part

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accession-icon GSE67766
Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE67628
The effect of SUZ12 knockdown on the responsivness of IFNg Stimulated Genes
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanWG-6 v3.0 expression beadchip

Description

We studied the effect of knowking down SUZ12 +/- knowckdown of BRM on the responsivness of IFNg stimulated genes. Cells were transfected with siSZU12+/-siBRM or control siRNA+/-siBRM. Cells were then left untreated or exposed to IFNg for 6 hours.

Publication Title

Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways.

Sample Metadata Fields

Cell line

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accession-icon GSE67626
The effect of BRG1 on the responsivness of IFNg Stimulated Genes
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

We studied the effect of reconstitution of BRG1 in BRG1-deficient cells on the responsivness of IFNg stimulated genes. Cells were infected with control adenovirus or BRG1-encoding virus. Cells were then left untreated or exposed to IFNg for 6 hours.

Publication Title

Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways.

Sample Metadata Fields

Cell line

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accession-icon GSE53658
shRNA kinome screen identifies TBK1 as therapeutic target for HER2+ breast cancer
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Microarray analysis was performed at the UHN Microarray Centre (UHNMAC, Ontario, Canada) using Illumina HumanHT-12 v4 BeadChip with 500 ng of total RNA prepared by RNeasy mini kit (QIAGEN, Cat. No. 74104). Samples from HCC1954 cells with 3-day treatment of TBK1-II at 4 uM were used to compare with vehicle-treated controls. Microarray data was processed and normalized by lumi package from BioConductor in R with Quantile Method. Difference between the samples were calculated by Bayesian statistic using limma package from BioConductor in R to obtain Moderated T value for subsequent Pathway analysis.

Publication Title

shRNA kinome screen identifies TBK1 as a therapeutic target for HER2+ breast cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE73073
Expression data comparing KRas(G12D/+);CreT, R26(H1047R/+);KRas(G12D/+);CreT, and MMTV-Neu mouse mammary tumors
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Breast Cancer (BC) has been associated with alterations in signaling through a number of growth factor and hormone regulated pathways. Mouse models for metastatic BC have been developed using oncoproteins that activate PI3K, Stat3 and Ras signaling. To determine the role of each pathway, we analyzed mouse mammary tumor formation when they were activated singly or pairwise.

Publication Title

Ras Signaling Is a Key Determinant for Metastatic Dissemination and Poor Survival of Luminal Breast Cancer Patients.

Sample Metadata Fields

Specimen part

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accession-icon GSE14596
HIV Integration analysis in quiescent CD4 T cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This study examines the sites of HIV integration in quiescent CD4 T cells and compares them to activated T cells. The expression patterns of the sites hosting integration events were determined using microarray analysis data from quiescent and activated CD4 T cells.

Publication Title

Human immunodeficiency virus integration efficiency and site selection in quiescent CD4+ T cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32939
CD4 on human monocytes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We examined the efffects of ligating CD4 expressed by primary human peripheral blood monocytes with soluble MHC Class II.

Publication Title

CD4 ligation on human blood monocytes triggers macrophage differentiation and enhances HIV infection.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE21987
Expression Profiling of Cellular Genes Modulated by Kaposis Sarcoma Associated Herpesvirus (KSHV) RTA/ORF50 in HEK293 Cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

KSHV RTA (K-RTA) is a transcriptional activator that functions to disrupt KSHV latency and activates specific sets of viral promoters in the lytic cycle. Structure-function studies indicate that K-RTA possesses a very potent transactivation domain locating at the C-terminus. To further characterize the biological functions of K-RTA, we have established three doxycycline-inducible K-RTA 293 cell lines using RevTRE/Tet-On system (Clontech). Comparing to two control lines in which K-RTA was replaced with luciferase reporter, a total of 88 host genes were identified to be modulated by 24 h doxycycline-induced K-RTA synthesized in 293 cells.

Publication Title

Gene expression and transcription factor profiling reveal inhibition of transcription factor cAMP-response element-binding protein by gamma-herpesvirus replication and transcription activator.

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)

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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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