Expression data of ES cells with or without Pcgf6, Ring1A/B, Max and Mga. Expression data of ES cells with or without Cbx1/3. Overall design: Mouse embryonic stem cells deficient for Pcgf6 and associating genes were evaluated using RNA-seq. Mouse embryonic stem cells deficient for Cbx1/3 and associating genes were evaluated using RNA-seq.
PCGF6-PRC1 suppresses premature differentiation of mouse embryonic stem cells by regulating germ cell-related genes.
Specimen part, Cell line, Treatment, Subject, Time
View SamplesTo gain insight into the signaling pathway(s) required for ABL1/ABL2-dependent non-small cell carcinoma cells metastasis Overall design: Samples were analyzed by pair of either control versus ABL Kinase inhibitor GNF5, Or using scrambled shRNA versus ABL1/ABL2-specific shRNAs.
Inactivation of ABL kinases suppresses non-small cell lung cancer metastasis.
No sample metadata fields
View SamplesEpithelial basal cells (BCs) are an important stem cell population of the airways. We purified BCs from a KRT5-GFP transgenic mouse line and used Affymetrix arrays to compare there gene expression to that of non-BC epithelium.
Basal cells as stem cells of the mouse trachea and human airway epithelium.
Specimen part, Cell line
View SamplesTranscriptomic characterization of cultured primary human cytrophoblasts (2nd trimester) undergoing differentiation/invasion in vitro.
Transcriptional Dynamics of Cultured Human Villous Cytotrophoblasts.
Specimen part
View SamplesIdiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease that is difficult to diagnose and follows an unpredictable clinical course. The object of this study was to develop a predictive gene signature model of IPF from whole lung tissue. We collected whole lung samples from 11 IPF patients undergoing diagnostic surgical biopsy or transplantation. Whenever possible, samples were obtained from different lobes. Normals consisted of healthy organs donated for transplantation. We measured gene expression on microarrays. Data were analyzed by hierarchical clustering and Principal Component Analysis. By this approach, we found that gene expression was similar in the upper and lower lobes of individuals with IPF. We also found that biopsied and explanted specimens contained different patterns of gene expression; therefore, we analyzed biopsies and explants separately. Signatures were derived by fitting top genes to a Bayesian probit regression model. We developed a 153-gene signature that discriminates IPF biopsies from normal. We also developed a 70-gene signature that discriminates IPF explants from normal. Both signatures were validated on an independent cohort. The IPF Biopsy signature correctly diagnosed 76% of the validation cases (p < 0.01), while IPF Explant correctly diagnosed 78% (p < 0.001). Examination of differentially expressed genes revealed partial overlap between IPF Biopsy and IPF Explant and almost no overlap with previously reported IPF gene lists. However, several overlapping genes may provide a basis for developing therapeutic targets.
Bayesian probit regression model for the diagnosis of pulmonary fibrosis: proof-of-principle.
Sex, Age, Specimen part
View SamplesTranscriptomic characterization of BDE-47 exposed cultured primary human cytrophoblasts (2nd trimester) undergoing differentiation in vitro.
Genomic Profiling of BDE-47 Effects on Human Placental Cytotrophoblasts.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Defective decidualization during and after severe preeclampsia reveals a possible maternal contribution to the etiology.
Sex, Age, Specimen part
View SamplesComparative analysis between oral and cutaneous wound healing in humans using paired and sequential biopsies during the repair process. Overall design: mRNA profiles of Oral/Skin Wound Healing human sample were generated by sequencing using Illumina
Transcriptional signature primes human oral mucosa for rapid wound healing.
Specimen part, Disease stage, Subject
View SamplesIn preeclampsia (PE), cytotrophoblast (CTB) invasion of the uterus and spiral arteries is often shallow. Thus, the placentas role has been a focus. We hypothesized that decidual defects are an important determinant of the placental phenotype. We isolated (human) endometrial stromal cells (hESCs) from non-pregnant donors with a prior pregnancy that was complicated by severe PE (sPE). Versus controls, they failed to decidualize as demonstrated by morphological criteria and the analysis of stage-specific antigens. These results were bolstered by showing that they were transcriptionally inert. Additionally, we used laser microdissection to isolate the decidua from tissue sections of the maternal-fetal interface. Transcriptional profiling revealed sPE-associated defects in gene expression. Also, decidual cells from sPE patients, which de-differentiated in vitro, failed to re-decidualize in culture. Immediately following isolation they released factors that inhibited CTB invasion, linking a possible cause to a known effect. These data suggested that failed decidualization is an important contributor to down regulated CTB invasion in sPE. Diagnosis of this defect prior to pregnancy would enable therapies that are designed to improve decidualization, a novel strategy for prevention.
Defective decidualization during and after severe preeclampsia reveals a possible maternal contribution to the etiology.
Specimen part
View SamplesPurpose: More than 90% of children with diffuse intrinsic pontine glioma (DIPG) die within 2 years of diagnosis. There is a dire need to identify therapeutic targets, however lack of patient material for research has limited progress. We evaluated a large cohort of diffuse intrinsic pontine gliomas (DIPGs) to identify recurrent genomic abnormalities and gene expression signatures underlying DIPG.
Genome-wide analyses identify recurrent amplifications of receptor tyrosine kinases and cell-cycle regulatory genes in diffuse intrinsic pontine glioma.
Age, Specimen part, Disease
View Samples