Allergic diseases correspond to a broad range of hypersensitivity reactions, often occurring as co-morbidities. Investigation of the molecular basis of allergy is a challenge because of its highly heterogeneous nature. We combined large-scale and high-throughput gene expression technology and systems biology approaches to retrieve relevant biomarkers and signalling pathways.
A novel whole blood gene expression signature for asthma, dermatitis, and rhinitis multimorbidity in children and adolescents.
Sex, Age, Specimen part
View SamplesAllergic diseases correspond to a broad range of hypersensitivity reactions, often occurring as co-morbidities. Investigation of the molecular basis of allergy is a challenge because of its highly heterogeneous nature. We combined large-scale and high-throughput gene expression technology and systems biology approaches to retrieve relevant biomarkers and signalling pathways.
A novel whole blood gene expression signature for asthma, dermatitis, and rhinitis multimorbidity in children and adolescents.
Sex, Age, Specimen part
View SamplesWe performed a transcriptomic analysis to identify genes differentially transcribed in the maize stem upon corn borer feeding and treatment with insects regurgitates by using the MACE (Massive Analysis of cDNA Ends) technology. Overall design: Two comparisons were performed: Insect chewing vs control and Regurgitate+wounding vs wounding in three biological replicates per treatment
Maize Stem Response to Long-Term Attack by <i>Sesamia nonagrioides</i>.
Specimen part, Treatment, Subject
View SamplesGene expression profiles of paired normal adjacent mucosa and tumor samples from 98 individuals and 50 healthy colon mucosae, were obtained through Affymetrix Human Genome U219 Arrays. This dataset is in the context of the COLONOMICS project and to query additional information you can visit the project website www.colonomics.org.
Discovery and validation of new potential biomarkers for early detection of colon cancer.
Sex, Age, Disease, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs in hematological malignancies.
Cell line, Treatment
View SamplesThe indisputable role of epigenetics in cancer and the fact that epigenetic alterations can be reversed have favored development of epigenetic drugs. In this study, we have design and synthesize potent novel, selective and reversible chemical probes that simultaneously inhibit the G9a and DNMTs methyltransferase activity. In vitro treatment of hematological neoplasia (Acute Myeloid Leukemia-AML, Acute Lymphoblastic Leukemia-ALL and Diffuse Large B-cell Lymphoma-DLBCL) with the lead compound CM-272, inhibited cell proliferation and promoted apoptosis, inducing interferon stimulated genes and immunogenic cell death. CM-272 significantly prolonged survival of AML, ALL and DLBCL xenogeneic models. Our results represent the discovery of first-in-class dual inhibitors of G9a/DNMTs and establish this chemical series, as a promising therapeutic tool for unmet needs in hematological tumors.
Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs in hematological malignancies.
Cell line, Treatment
View SamplesThe aim of this study was to establish an in vitro model to investigate the initial stages of human implantation based on co-culture of a) immortalized cells representing the receptive (Ishikawa) or non-receptive (HEC-1-A) endometrial epithelium with b) spheroids of a trophoblastic cell line (JEG-3) modified to express green fluorescent protein. After co-culturing Ishikawa cells with trophoblast spheroids, 310 and 298 genes increased or decreased their expression compared to non-co-cultured Ishikawa control cells, respectively; only 9 genes (5 increased and 4 decreased) were differentially expressed in HEC-1-A upon co-culture with trophoblast spheroids. Compared to HEC-1-A, the trophoblast challenge to Ishikawa cells differentially regulated the expression of 495 genes. In summary, upon co-culture with the trophoblast spheroids, non-receptive epithelium is characterized by a muted transcriptional response which in turn fails to activate the full transcriptional response that trophoblast spheroids undergo when co-cultured with receptive epithelium. Overall design: GFP expressing JEG-3 spheroids were co-cultured with confluent monolayers of receptive Ishikawa or non-receptive HEC-1-A epithelia. After 48 hours of co-culture, GFP+ (trophoblast JEG-3 spheroid cells) and GFP- cell fractions (receptive Ishikawa or non-receptive HEC-1-A epithelial cells) were isolated by fluorescence-activated flow cytometry (FACS). The specific transcriptional changes of the isolated cell populations were analyzed by RNA-seq profiling. Statistical significance of gene expression differences was set at an absolute log2 fold change (log2FC) =1 and an adjusted p-value <0.05.
Transcriptomic analysis of the interaction of choriocarcinoma spheroids with receptive vs. non-receptive endometrial epithelium cell lines: an in vitro model for human implantation.
Specimen part, Subject
View SamplesWe show that the epididymal white adipose tissue harbors 4 subpopulations of macrophages (VAM1, VAM2, PreVAM and DPs), 2 subpopulations of Dendritic Cells (CD11B+CD103- and CD11B-CD103+) and monocytes. VAMs display a gene signature enriched in pathways related to anti-inflammatory/ detoxifying and repair processes. Our gene expression work shows no evidence of an M2 to a Classically Activated/M1 shift during diet-induced obesity (DIO). Gene expression of VAMs or DP macrophages cannot be defined as M1 or M1-like. Our data are more compatible with the category of “Metabolically-activated” macrophages (MMe) Overall design: Examination of RNA expression changes in different epididymal adipose tissue myeloid subpopulations in lean versus obese animals harboring metabolic syndrome
Vasculature-associated fat macrophages readily adapt to inflammatory and metabolic challenges.
Cell line, Subject
View SamplesBladder cancer (BC) is a highly prevalent human disease in which Rb pathway inactivation and epigenetic alterations are common events. However, the connection between these two processes is still poorly understood. Here we show that the in vivo inactivation of all Rb family genes in the mouse urothelium is sufficient to initiate BC development. The characterization of the mouse tumors revealed multiple molecular features of human BC, including the activation of E2F transcription factor and subsequent Ezh2 expression, and the activation of several signaling pathways previously identified as highly relevant in urothelial tumors. Whole transcriptional characterizations of the mouse bladder tumors revealed a significant overlap with human BC samples, and a predominant role for Ezh2 in the downregulation of gene expression programs. Importantly, we determined that in human superficial BC patients, the increased tumor recurrence and progression in these recurrences is associated with increased E2F and Ezh2 expression and Ezh2-mediated gene expression repression. Collectively, our studies provide a genetically defined model for human high-grade superficial BC and demonstrate the existence of an Rb-E2F-Ezh2 axis in bladder whose disruption can promote tumor development.
In vivo disruption of an Rb-E2F-Ezh2 signaling loop causes bladder cancer.
Specimen part, Disease, Treatment
View SamplesDifferent mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons.
RNA microarray analysis in prenatal mouse cochlea reveals novel IGF-I target genes: implication of MEF2 and FOXM1 transcription factors.
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