To identify sex-based differences in gene pathways affected by endgoenous genomic instaiblity resulting in embryonic death, total RNA from E13.5 placentas was isolated for RNAseq. Placentas from male and female embryos from wild-type matings and Mcm4^C3/C3 homozygous matings were used as references. Male and female placentas derived from embryos of the genotype : Mcm4^C3/C3 Mcm2^Gt/+ from either male Mcm4^C3/+ Mcm2^Gt/+ crossed to female Mcm4^C3/C3 or male Mcm4^C3/C3 crossed to female Mcm4^C3/+ Mcm2^Gt/+ were the experimental samples. Overall design: Total RNA was isolated from E13.5 placentas and subjected to directional RNAseq to identify sex-based transciptome differences.
Female-biased embryonic death from inflammation induced by genomic instability.
Specimen part, Cell line, Subject
View SamplesThe goal of this study was to identify important genetic pathways that are altered in mammary tumor cells upon over-expression of the tumor suppressor gene Arid1a. The results of this experiment revealed that Arid1a helps regulate key cell-cycle checkpoint and growth regulatory pathways, either directly or indirectly. This helped explain in part the significant decrease in cell proliferation and tumor growth phenotypes observed both in vitro and in vivo, when comparing the same samples analyzed here by RNA-seq (untransduced replicates vs. add-back clonal lines). Overall design: Whole transcriptome comparison of mammary tumor cells derived from Chaos3 mouse model (23116 MT- control) vs. add-back clones overexpressing Arid1a (AB-C1 & AB-C2 - exp). Control and experimental samples were run in duplicate.
The Chromatin Remodeling Component Arid1a Is a Suppressor of Spontaneous Mammary Tumors in Mice.
Specimen part, Cell line, Subject
View SamplesAim: To discovery biomarkers in JIA base on gene expression from RNA sequencing on PBMC Method: Paired-end Ilumina sequencing to capture gene expression of PBMC from JIA individuals and healthy controls Results:sample heterogeneity makes RNA sequencing on PBMC unsuitable as a first-step method for screening biomarker candidates in JIA Overall design: RNA sequencing on PBMC of 3 independent cohorts consist of JIA patients and healthy controls
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Specimen part, Disease stage, Subject
View SamplesAim: To discovery biomarkers in JIA base on gene expression from RNA sequencing on CD4+ T Cells Method: Paired-end Ilumina sequencing to capture gene expression of CD4+ T cells from JIA individuals with active disease and patients in clinical remission on medication. Overall design: RNA sequencing on CD4+T cells consist of JIA patients
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Specimen part, Disease stage, Subject
View SamplesExposure to vanadium pentoxide (V2O5) is a cause of occupational bronchitis. We evaluated gene expression profiles in cultured human lung fibroblasts exposed to V2O5 in vitro in order to identify candidate genes that could play a role in airway remodeling associated with V2O5-induced bronchitis. Gene expression was measured at various time points over a 24 hr period using the Affymetrix Human Genome U133A 2.0 Array. Expression data were preprocessed using RMA with a log2 transformation. Statistical analysis was performed in R using the affylmGUI package using a linear model with contrasts between untreated control and V2O5-exposed fibroblasts. Genes identified as statistically significant were filtered by selecting only those genes that exhibited a > 2-fold change. Quantitative real-time RT-PCR was utilized to confirm expression of selected genes. More than 2000 genes were significantly changed in response to V2O5 over the time course of our experiment. Genes altered by V2O5 were involved in biologic processes related to cell growth and differentiation, oxidative stress responses, immune regulation, and interferon signaling and apoptosis. In particular, V2O5 induced genes that encode growth factors involved in epithelial repair (HB-EGF) or angiogenesis (VEGF), peroxide generating enzymes (SOD2), pro-inflammatory enzymes (PGHS2), while suppressing genes involved in growth arrest (GAS1, STAT-1) and cell cycle inhibition (CDKN1B). Our study also identified a variety of novel genes that could be used as biomarkers of V2O5-induced bronchitis or could serve as candidate genes for disease progression.
Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify candidate genes for occupational bronchitis.
No sample metadata fields
View SamplesWnt signaling in early eye development, specifically the lens placode shows expression of 12 out of 19 Wnt ligands. We these Wnt activities were suppressed using conditional deletion of Wntless, dramatic phenotypic changes in morphogensis occurred.
Wnt ligands from the embryonic surface ectoderm regulate 'bimetallic strip' optic cup morphogenesis in mouse.
Specimen part
View SamplesWe report single-cell transcriptional assessment and functional circuit characterization of neuron types within the mouse entopeduncular nucleus (EP) Overall design: Transcriptional profilingof EP neurons from P60-70 C57BL/6 male mice; three types were identified, characterized, and incorporated into a synaptic-circuit model of basal ganglia please note that Replicate 2 was lost experimentally and not included, so n=3 replicates total
Genetically Distinct Parallel Pathways in the Entopeduncular Nucleus for Limbic and Sensorimotor Output of the Basal Ganglia.
Sex, Specimen part, Cell line, Subject
View SamplesThe incidence and mortality rates of prostate cancer are significantly higher in African-American men when compared to European-American men. We tested the hypothesis that differences in tumor biology contribute to this survival health disparity. Using microarray technology, we obtained gene expression profiles of primary prostate tumors resected from 33 African-American and 36 European-American patients. These tumors were matched on clinical parameters. We also evaluated 18 non-tumor prostate tissues from 7 African-American and 11 European-American patients. The resulting datasets were analyzed for expression differences on the gene and pathway level comparing African-American with European-American patients. Our analysis revealed a significant number of genes, e.g., 162 transcripts at a false-discovery rate less than 5%, to be differently expressed between African-American and European-American patients. Using a disease association analysis, we identified a common relationship of these transcripts with autoimmunity and inflammation. These findings were corroborated on the pathway level with numerous differently expressed genes clustering in immune response, stress response, cytokine signaling, and chemotaxis pathways. Furthermore, a two-gene tumor signature was identified that accurately differentiated between African-American and European-American patients. This finding was confirmed in a blinded analysis of a second sample set. In conclusion, the gene expression profiles of prostate tumors indicate prominent differences in tumor immunobiology between African-American and European-American men. The profiles portray the existence of a distinct tumor microenvironment in these two patient groups.
Tumor immunobiological differences in prostate cancer between African-American and European-American men.
Race
View SamplesNeuroblastoma (NBL) is an embryonal cancer of the sympathetic nervous system (SNS) that causes 15% of pediatric cancer deaths. High-risk neuroblastoma is characterized by N-Myc amplification and segmental chromosomal gains and losses. Due to limited disease models, the etiology of neuroblastoma is largely unknown, including both the cell of origin and the majority of oncogenic drivers. We have established a novel system for studying neuroblastoma based on the transformation of neural crest cells (NCCs), the progenitor cells of the SNS, isolated from mouse embryonic day 9.5 trunk neural tube explants. Based on pathology and gene expression analysis, we report the first successful transformation of wild-type NCCs into NBL by enforced expression of N-Myc to generate phenotypically and molecularly accurate tumors that closely model human MYCN-amplified NBL. Using comparative genomic hybridization, we found that NCC-derived neuroblastoma tumors acquired copy number gains and losses that are syntenic to those observed in human MYCN-amplified neuroblastoma including 17q gain, 2p gain and loss of 1p36. When p53-compromised NCCs were transformed with N-Myc we generated primitive neuroectodermal tumors with divergent differentiation including osteosarcoma. These subcutaneous tumors were metastatic to regional lymph nodes, liver and lung. Our novel experimental approach accurately models human neuroblastoma and establishes a new system with potential to study early stages of neuroblastoma oncogenesis, to functionally assess neuroblastoma oncogenic drivers, and to characterize neuroblastoma metastasis.
MYCN induces neuroblastoma in primary neural crest cells.
Specimen part
View SamplesAppropriate bone mass is maintained by the actions of the main cells in the bone, osteoclasts and osteoblasts. The Stat3 transcription factor is known to have an effect on maintaining bone mass, but it is not known whether its key actions are in osteoblasts, osteoclasts, or both. Preliminary data indicated that Stat3 plays a role in osteoclast differentiation, but the mechanisms of this role are not yet understood.
The loss of STAT3 in mature osteoclasts has detrimental effects on bone structure.
Cell line
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