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Mus musculus
7 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The human SYT-SSX fusion protein was expressed in a developmentally dependent fashion in murine myoblasts. Tumors harvested from mice in adolescence were compared to normal mouse skeletal muscle samples.
Publication Title
A conditional mouse model of synovial sarcoma: insights into a myogenic origin.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus, Homo sapiens
- 16 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip, Illumina HumanWG-6 v3.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
High-grade serous ovarian cancer arises from fallopian tube in a mouse model.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
We analyzed gene expression in human fibroblasts stimulated by platelet-derived growth factor-BB (PDGF-BB) or basic fibroblast growth factor (bFGF) for 1h and 24h. The results of two independent experiments were merged. SAM analysis identified 116 relevant probe sets. Hierarchical clustering of these probe sets showed divergent early gene regulation by PDGF and FGF but overlapping late response. We first analyzed genes commonly regulated by PDGF-BB and b-FGF more than 2 fold after 24h of stimulation and we found that these two growth factors repressed FOXO.
Publication Title
The transcription of FOXO genes is stimulated by FOXO3 and repressed by growth factors.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Illumina HumanWG-6 v3.0 expression beadchip
Description
The cell of origin of serious ovarian cancer is unknown. To create a mouse model for this lethal cancer and identify early cancer biomarkers, we conditionally deleted both Dicer (essential for microRNA biosynthesis) and Pten (a negative regulator of the PI3K pathway) in the female reproductive tract. Beginning at ~3-5 months, these Dicer/Pten mutant mice develop high-grade serious carcinomas that initiate in the stroma of the fallopian tube through a mesenchymal-to-epithelial transition (MET), subsequently envelop the ovary, and then metastasize throughout the peritoneum, resulting in ascites and 100% lethality by 13 months. The fallopian tube cancers demonstrate upregulation of genes encoding known and novel secreted proteins that are potential biomarkers. This study uncovers a new paradigm for the initiation of high-grade serous ovarian cancer.
Publication Title
High-grade serous ovarian cancer arises from fallopian tube in a mouse model.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip, Illumina HumanWG-6 v3.0 expression beadchip
Description
The cell of origin of serious ovarian cancer is unknown. To create a mouse model for this lethal cancer and identify early cancer biomarkers, we conditionally deleted both Dicer (essential for microRNA biosynthesis) and Pten (a negative regulator of the PI3K pathway) in the female reproductive tract. Beginning at ~3-5 months, these Dicer/Pten mutant mice develop high-grade serious carcinomas that initiate in the stroma of the fallopian tube through a mesenchymal-to-epithelial transition (MET), subsequently envelop the ovary, and then metastasize throughout the peritoneum, resulting in ascites and 100% lethality by 13 months. The fallopian tube cancers demonstrate upregulation of genes encoding known and novel secreted proteins that are potential biomarkers. This study uncovers a new paradigm for the initiation of high-grade serous ovarian cancer.
Publication Title
High-grade serous ovarian cancer arises from fallopian tube in a mouse model.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 55 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The goal of this study is to identify downstream pathways, diagnostic markers, and potential therapeutic targets for IFS/CMN.
Publication Title
Mediators of receptor tyrosine kinase activation in infantile fibrosarcoma: a Children's Oncology Group study.
Sample Metadata Fields
Specimen part
View Samples
GSE99561- Mus musculus, Unidentified
- 267 Downloadable Samples
Illumina HiSeq 2000, Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Systems genetics identifies a co-regulated module of liver microRNAs associated with plasma LDL cholesterol in murine diet-induced dyslipidemia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus, Unidentified
- 267 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st), Illumina HiSeq 2000
Description
Genetic variation, in addition to environmental influences like diet, can govern the expression levels of microRNAs (miRNAs). MiRNAs are commonly found to operate cooperatively in groups to regulate gene expression. To investigate this, we combined small RNA sequencing, clinical phenotypes, and microarray data measuring gene expression from an outbred mouse model, the Diversity Outbred population. In the DO population, each individual has a distinct genome that is a mosaic of 8 inbred founder strains. We used these data to identify co-regulated modules of miRNAs and genes that are influenced by genetics and diet, and identify relationships between the modules and phenotypes in over 200 DO mice.
Publication Title
Systems genetics identifies a co-regulated module of liver microRNAs associated with plasma LDL cholesterol in murine diet-induced dyslipidemia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
High-throughput genomic studies have identified thousands of genetic alterations in colorectal cancer (CRC). Distinguishing driver from passenger mutations is critical for developing rational therapeutic strategies. Because only a few transcriptional subtypes exist in previously studied tumor types, we hypothesize that highly heterogeneous genomic alterations may converge to a limited number of distinct mechanisms that drive unique gene expression patterns in different transcriptional subtypes. In this study, we defined transcriptional subtypes for CRC and identified driver networks/pathways for each subtype, respectively. Applying consensus clustering to a patient cohort with 1173 samples identified three transcriptional subtypes, which were validated in an independent cohort with 485 samples. The three subtypes were characterized by different transcriptional programs related to normal adult colon, early colon embryonic development, and epithelial mesenchymal transition, respectively. They also showed statistically different clinical outcomes. For each subtype, we mapped somatic mutation and copy number variation data onto an integrated signaling network and identified subtype-specific driver networks using a random walk-based strategy. We found that genomic alterations in the Wnt signaling pathway were common among all three subtypes; however, unique combinations of pathway alterations including Wnt, VEGF, Notch and TGF-beta drove distinct molecular and clinical phenotypes in different CRC subtypes. Our results provide a coherent and integrated picture of human CRC that links genomic alterations to molecular and clinical consequences, and which provides insights for the development of personalized therapeutic strategies for different CRC subtypes.
Publication Title
Deciphering genomic alterations in colorectal cancer through transcriptional subtype-based network analysis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
To provide insight into the role of and target genes of the transcription factor FOXP1 in mature human B cells and in B cell non-Hodkgin lymhomas, we performed gene expression microarray studies, upon ectopic overexpression or silencing of FOXP1 in these cells.
Publication Title
FOXP1 directly represses transcription of proapoptotic genes and cooperates with NF-κB to promote survival of human B cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples