We obtained radiographically-localized biopsies during glioma resection surgeries to sample the tumor core and margins from multiple glioma patients. We also procured fresh, non-neoplastic brain tissue specimens from multiple patients having procedures to relieve epilespy symptoms or to place shunts to treat normal pressure hydrocephalus. We then used RNA-Seq to compare expression patterns between geographically distinct regions of gliomas and computational deconvolution to estimate cell type-specific expression patterns in different disease subtypes. Overall design: RNA-Seq analysis in 39 contrast-enhancing glioma core samples, 36 non-enhancing FLAIR glioma margin samples, and 17 non-neoplastic brain tissue samples.
MRI-localized biopsies reveal subtype-specific differences in molecular and cellular composition at the margins of glioblastoma.
No sample metadata fields
View SamplesIMP3 (IGF2-mRNA binding protein 3) is a member of a family of IGF2-mRNA binding proteins that function in RNA stabilization, trafficking and localization. It exhibits the properties of an oncofetal protein and its expression correlates with the aggressive behavior of many tumors. In breast cancer, IMP3 is associated with the highly aggressive triple-negative subtype (TNBC) The challenge is to identify specific proteins and functions that are regulated by IMP3. As an approach to this problem, we compared the mRNA expression profile of SUM-1315 cells, a TNBC cell line, to the same cells that had been depleted of IMP3. Overall design: SUM-1315 breast cancer cells were were infected with lentivirus for control shRNA and two different IMP3 shRNAs and processed for RNA-sequencing
IMP3 Stabilization of WNT5B mRNA Facilitates TAZ Activation in Breast Cancer.
Specimen part, Subject
View SamplesThe goal of this study was to compare mRNA from mammary epithelial cells of 3 mammary-specific Nmi knockout FVB with corresponding wildtype control. This was performed to obtain clues to the signaling pathways that were impacted in the mammary epithelial cells upon knocking-out Nmi expression. Overall design: To determine how the loss of Nmi contributed to a hyper-proliferative phenotype during puberty and lactation, we performed global RNAseq analysis from enriched mammary epithelial organoids from lactation day1 (L1), the time when Nmi protein expression in normal mammary epithelium is at its highest level. We compared 2 groups with 3 mice/group. We used second and third mammary glands of each mouse. These glands were isolated from mice on the first day of lactation, minced and dissociated in digestion medium (HBSS containing collagenase I (Sigma Aldrich, St. Louis, MO) (1mg/mL) and Pronase (Sigma Aldrich) (0.1mg/mL)) for two hours at 37C with shaking. Epithelial organoids were washed in PBS and enriched by pulse centrifugation to 1500rpm at least three times before subsequent assays.
Conditional knockout of N-Myc and STAT interactor disrupts normal mammary development and enhances metastatic ability of mammary tumors.
Specimen part, Subject
View SamplesNatural killer T (NKT) cells have immune stimulatory or inhibitory effects on the immune response that are context-dependent. This may be attributed in part to the existence of functional NKT cell subsets; however, these functional subsets have only been characterized on the basis of differential expression of a few transcription factors and cell surface molecules. Here we have analyzed purified populations of thymic NKT cell subsets at both the transcriptomic and epigenomic levels, and by single-cell RNA sequencing. Our data indicate that despite their similar antigen specificity, the functional NKT cell subsets are highly divergent populations characterized by many gene expression and epigenetic differences. Therefore the thymus imprints innate-like NKT cells with novel combinations of properties, including differences in proliferative capacity, homing, and effector functions that were not previously anticipated. Overall design: Analysis of single cell transcriptomic heterogeneity in mouse Va14 iNKT thymocyte subsets (NKT1, NKT2, NKT17 and NKT0). Samples were generated from individual experiment using a pool of thymocytes prepared from five five-week old C57BL/6J females. NKT cells subtypes were isolated from thymuses and directly sorted by flow cytometry into lysis buffer (96 well plate single cell sort). The preparation of samples occurred in 2 different batches (both having a equal representation of the different cell populations).
Innate-like functions of natural killer T cell subsets result from highly divergent gene programs.
Sex, Age, Specimen part, Cell line, Subject
View Samples5 strains of rat, WKY, spontaneously hypertensive rat (SHR) and 3 reciprocal congenic strains (WconSA, SconSA and SISA) were used to generate expression data across the genome using the Affymetrix rat genome chip set comprising the 230 A and 230 B chips. 5 animals from each strain were used. Expression data was determined for 2 ages: 6 week and 24 week with whole kidney RNA.
Genetic dissection of a blood pressure quantitative trait locus on rat chromosome 1 and gene expression analysis identifies SPON1 as a novel candidate hypertension gene.
Age, Specimen part
View SamplesThe hemibiotrophic fungal pathogen Colletotrichum graminicola is the causal agent of anthracnose disease on maize stalks and leaves. After the formation of appressoria the host cell wall is penetrated by the conversion of appressorial turgor pressure into forceful ejection of a penetration peg. Subsequently, C. graminicola establishes biotrophic hyphae in the penetrated epidermis cell at around 36 hours post inoculation (hpi) until a switch of hyphal morphology and lifestyle takes place during the colonization of neighboring host cells at around 72 hpi. During the ensuing necrotrophic growth, dark necrotic lesions are formed that are visible as anthracnose symptoms. We used microarrays to detail the global programme of gene expression during the infection process of Colletotrichum graminicola in its host plant to get insight into the defense response of this compatible interaction and into the metabolic reprogramming needed to supply the fungus with nutrients.
Common Motifs in the Response of Cereal Primary Metabolism to Fungal Pathogens are not Based on Similar Transcriptional Reprogramming.
Time
View SamplesCHOPS syndrome is caused by germline gain-of-function mutations of AFF4. Cornelia de Lange syndrome is caused by germline mutations of cohesin loading factors or cohesin complex genes such as NIPBL, SMC1A, SMC3 and HDAC8. There are many overlapping clinical features exist between CHOPS syndrome and Cornelia de Lange syndrome. To identified commonly dysregulated genes in CHOPS syndrome and Cornelia de Lange syndrome, we perfomred side-by-side transcriptome comparison between CHOPS syndrome and Cornelia de Lange syndrome.
Germline gain-of-function mutations in AFF4 cause a developmental syndrome functionally linking the super elongation complex and cohesin.
Specimen part, Disease, Disease stage
View SamplesAFF4 is a component of super elongation complex (SEC), which plays an important role in mobilizing paused RNA polymerase II at gene promoter regions. Using exome sequenging, we have identified a novel genetic disorder caused by missense mutations in AFF4. We propose CHOPS syndrome as a name for this new diagnosis. To evaluate the effect of identified missense mutations of AFF4, utilizing patient derived skin fibroblast cell lines, the gene expression analysis was perfomred.
Germline gain-of-function mutations in AFF4 cause a developmental syndrome functionally linking the super elongation complex and cohesin.
Specimen part, Disease, Disease stage
View SamplesMetastatic melanoma is a deadly disease while non-metastatic melanoma and other cutaneous tumor types are usually cured with surgical removal of the primary tumors. This study evaluated gene expresion to determine if gene expression differences existed which would allow one to identify the metastatic tumors based on the expression of specific genes.
The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis.
No sample metadata fields
View SamplesThe bovine chromaffin cell (BCC) is a unique modela highly homogeneous and accessible neuroendocrine cellin which to study gene regulation through first messenger-initiated signaling pathways that are specific to post-mitotic cells. BCCs were treated with tumor necrosis factor (TNF) or pituitary adenylate cyclase activating polypeptide (PACAP), two critical regulators of neural cell transcriptional programming during inflammation that act on TNFR2 and PAC1 receptors, respectively, in post-mitotic neuroendocrine cells. Transcripts which were significantly up regulated by either or both first messenger were identified from microarray analysis using two bovine oligonucleotide arrays (Affymetrix and Agilent) followed by statistical analysis with Partek Genomic suite. Microarray data were combined from the two arrays using qRT-PCR sampling validation, and the first-messenger transcriptome derived from TNF and PACAP signaling were compared. More than 90 percent of the genes up regulated either by TNF or PACAP were specific to a single first messenger. BioBase suite, DIRE and Opossum were used to identify common promoter/enhancer response elements that control the expression of TNF- or PACAP-stimulated genes. Bioinformatic analysis revealed that distinct groups of transcription factors control the expression of genes up regulated by either TNF or PACAP . Most of the genes up regulated by TNF contained response elements for members of the Rel transcription factor family, suggesting TNF-TNFR2 signaling mainly through the NF-kB signaling pathway. On the other hand, the PACAP regulated genes showed no enrichment for any single response element, containing instead response elements for combinations of transcription factors allowing activation through multiple signaling pathways, including cAMP, calcium and ERK, in neuroendocrine cells. Pharmacological strategies for mimicking neuroprotection by either PACAP or TNF in the context of CNS injury or degeneration in disease might focus on individual downstream gene activation pathways to achieve greater specificity in vivo.
Neuropeptides, growth factors, and cytokines: a cohort of informational molecules whose expression is up-regulated by the stress-associated slow transmitter PACAP in chromaffin cells.
Specimen part
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