RNA sequencing analysis of gene expression in serrated colon polyps, uninvolved colon and control colon Overall design: 86 colon RNA sequencing datasets (21 sessile serrated adenomas/polyps, 10 hyperplastic polyps, 10 adenomatous polyps, 21 uninvolved colon, 20 control colon and 4 colon cancer)
Gene Signature in Sessile Serrated Polyps Identifies Colon Cancer Subtype.
No sample metadata fields
View SamplesTo assess natural variation of downstream auxin responses we subjected 7 different arabidopsis ecotypes to a time course of auxin treatments. 7d-old seedlings grown in liquid culture have been treated for 0, 30 min, 1h and 3h with 1 M IAA.
Natural variation of transcriptional auxin response networks in Arabidopsis thaliana.
Specimen part
View SamplesRNA-sequencing of SSP RNA from patients with serrated polyposis syndrome identifies VSIG1 and MUC17 as potential diagnostic markers for SSPs Overall design: 5'' capped RNA from seven ascending SSPs, six patient matched uninvolved right colon and two normal right colon samples was used for RNA sequencing (15 samples total)
RNA sequencing of sessile serrated colon polyps identifies differentially expressed genes and immunohistochemical markers.
Sex, Disease, Subject
View SamplesAnalysis of alveolar macrophage gene expression in C57BL6 wild-type and RAGE null mice exposed to cigarette smoke Overall design: 4 groups of 3-4 mice at two exposure time points (7-day and 4 month), 31 samples total
RAGE is a Critical Mediator of Pulmonary Oxidative Stress, Alveolar Macrophage Activation and Emphysema in Response to Cigarette Smoke.
Cell line, Subject, Time
View SamplesWe demonstrate that expression of key markers of keratinocyte differentiation is suppressed by exposure to sodium arsenite. Folate deficiency exacerbates this effect. In addition, cancer-related cell movement genes, and growth and proliferation genes are altered. Several redox-sensitive transcription factors are implicated in mediating these gene expression changes due to arsenic treatment and folate deficiency.
Folate deficiency enhances arsenic effects on expression of genes involved in epidermal differentiation in transgenic K6/ODC mouse skin.
No sample metadata fields
View SamplesAnalysis of hepatic gene expression in mice transiently overexpressing Bcl2 Overall design: 3 control GFP mice and 5 GFP-Bcl2 mice, 8 mouse liver samples total
Bcl2 is a critical regulator of bile acid homeostasis by dictating Shp and lncRNA H19 function.
No sample metadata fields
View SamplesRNA sequencing of duodenal polyps in FAP patients treated with plabebo or the drug combination, erlotinib + sulindac Overall design: 69 duodenal RNA sequencing datasets (17 baseline uninvolved from 17 FAP patients, 10 endpoint uninvolved and 16 polyp from 10 FAP patients on placebo, 10 endpont uninvolved and 16 polyp from 10 FAP patients on drug)
Chemoprevention with Cyclooxygenase and Epidermal Growth Factor Receptor Inhibitors in Familial Adenomatous Polyposis Patients: mRNA Signatures of Duodenal Neoplasia.
Specimen part, Treatment, Subject, Time
View SamplesThe cellular origin of Ewing tumor (ET), a tumor of bone or soft tissues characterized by specific fusions between EWS and ETS genes, is highly debated. Through gene expression analysis comparing ETs with a variety of normal tissues, we show that the profiles of different EWS-FLI1-silenced Ewing cell lines converge toward that of mesenchymal stem cells (MSC). Moreover, upon EWS-FLI1 silencing, two different Ewing cell lines can differentiate along the adipogenic lineage when incubated in appropriate differentiation cocktails. In addition, Ewing cells can also differentiate along the osteogenic lineage upon long-term inhibition of EWS-FLI1. These in silico and experimental data strongly suggest that the inhibition of EWS-FLI1 may allow Ewing cells to recover the phenotype of their MSC progenitor.
Mesenchymal stem cell features of Ewing tumors.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Distinct cachexia profiles in response to human pancreatic tumours in mouse limb and respiratory muscle.
Specimen part, Treatment
View SamplesBackground: Cancer cachexia is a life-threatening metabolic syndrome that causes significant loss of skeletal muscle mass and significantly increases mortality in cancer patients. Currently, there is an urgent need for better understanding of the molecular pathophysiology of this disease, so that effective therapies can be developed. Almost all pre-clinical studies evaluating skeletal muscle’s response to cancer have focused on one or two pre-clinical models, and almost all have focused specifically on limb muscles. In the current study, we reveal key differences in the histology and transcriptomic signatures of a limb muscle and a respiratory muscle in orthotopic pancreatic cancer patient-derived xenograft (PDX) mice. Methods: To create the four cohorts of PDX mice evaluated in this study, tumors resected from four pancreatic ductal adenocarcinoma (PDAC) patients were portioned and attached to the pancreas of immunodeficient NSG mice. Results: Body weight, muscle mass, and fat mass were significantly decreased in each PDX line. Histological assessment of cryosections taken from the tibialis anterior (TA) and diaphragm (DIA) revealed differential effects of tumor-burden on their morphology. Subsequent genome-wide microarray analysis on TA and DIA revealed key differences between their transcriptomes in response to cancer as well. Indeed, upregulated genes in the diaphragm were enriched for extracellular matrix (ECM) protein-encoding genes and genes related to the inflammatory response, and downregulated genes were enriched for mitochondria related protein-encoding genes. Conversely, the TA showed upregulation of canonical atrophy-associated pathways such as ubiquitin-mediated protein degradation and apoptosis and enrichment of downregulated genes encoding ECM proteins. Conclusions: These data suggest that distinct biological processes account for wasting in different skeletal muscles in response to the same tumor burden. Further investigation into these differences will be critical for the future development of effective clinical strategies to counter cancer cachexia.
Distinct cachexia profiles in response to human pancreatic tumours in mouse limb and respiratory muscle.
Specimen part, Treatment
View Samples