This SuperSeries is composed of the SubSeries listed below.
Effects of maternal obesity on Wharton's Jelly mesenchymal stromal cells.
Specimen part, Subject
View SamplesA transcriptome signature which discriminate efficiently primary and radiation induced breast angiosarcomas can be generated from FFPE tumor samples.FFPE samples are good material to unlock relevant informations from tumors.
No associated publication
Specimen part
View SamplesWe showed that a large number of genes and exons were deregulated in colorectal adenomas in comparison with colorectal normal mucosa.
A gene expression and pre-mRNA splicing signature that marks the adenoma-adenocarcinoma progression in colorectal cancer.
Specimen part
View Samples7 WJ-MSC lines from non-obese BMI <25 kg/m2 were compared with 7 WJ-MSC lines obese BMI >30 kg/m2. No template was used as a negative control
No associated publication
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Human induced pluripotent stem cells as a tool to model a form of Leber congenital amaurosis.
Sex, Specimen part, Cell line
View SamplesThe aim of this study was to characterize the stroma displayed by different models of breast cancer tumors in mice. For this purpose, transcriptomic and flow cytometry analyses on murine populations were performed in a series of 25 PDXs and 2 most commonly used GEMs (MMTV-PyMT and MMTV-erBb2). Specifically, macrophages from 5 models were sorted and profiled by gene expression and phenotypically characterized by flow cytometry.
Characterization of Breast Cancer Preclinical Models Reveals a Specific Pattern of Macrophage Polarization.
Specimen part, Subject
View SamplesAcquired resistance to endocrine therapy occurs with high frequency in patients with luminal breast cancer (LBC). We report here the establishment of four patient-derived xenograft models of LBC with acquired resistance in vivo to tamoxifen and estrogen deprivation.
Acquired resistance to endocrine treatments is associated with tumor-specific molecular changes in patient-derived luminal breast cancer xenografts.
Specimen part
View SamplesThis work focuses on understanding the molecular basis of the immune dysfunctions in Idiopathic CD4+ T cells lymphocytopenia (ICL). ICL is a rare haematological disorder of unknown origin, characterized by a profound and persistent CD4+ T-cell defect, which predisposes to life threatening opportunistic infections very similar to those seen in AIDS. To analyse more in depth the functional pathways involved in ICL pathogenesis, we conducted gene expression profiling of CD4+ T-cells isolated from blood samples from ICL, sarcoidosis and healthy individuals. Our analyses have revealed specific CD4+ T-cells gene expression signatures in ICL associated with defective TCR activation threshold, expansion of the Treg-cell compartment and interestingly with accelerated immune aging.
DUSP4-mediated accelerated T-cell senescence in idiopathic CD4 lymphopenia.
Sex
View SamplesOur purpose was to investigate genes and molecular mechanisms involved in patients with Leber congenital amaurosis (LCA). Fibroblasts from two unrelated clinically-identified patients (Coriell) were reprogrammed to pluripotency by retroviral transduction. These human induced Pluripotent Stem Cells (hiPSCs) were differentiated into neural stem cells (NSC) that mimicked the neural tube stage and retinal pigmented epithelial (RPE) cells that could be targeted by the disease. A genome wide transcriptome analysis was performed with Affymetrix Exon Array GeneChip, comparing LCA-hiPSCs derivatives to controls. The aim was to identify differentially expressed genes which may be associated with early developmental defect before the establishment of mature retinal circuitry.
Human induced pluripotent stem cells as a tool to model a form of Leber congenital amaurosis.
Sex, Specimen part, Cell line
View SamplesWe performed exon array analysis to define and compare the transcriptomic changes, in terms of splicing and gene expression profilings, occurring in human neuroblastoma cells upon knocking down TDP-43 and FUS RNA-binding proteins (RBP), with the final aim to unravel the biological role of these RBPs in neuronal cells.
No associated publication
Cell line, Treatment
View Samples