Investigating the effects of two different classes of KDM1A inhibitors on the transcriptome of AML cell lines Overall design: 16 different samples with biological replicates. Treatment for 24 and 72 hours with an irreversible KDM1A inhibitor (RN-1) or a reversible KDM1A inhibitor (GSK690) or an inactive isomer of the latter (GSK690*).
Pharmacological Inhibition of the Histone Lysine Demethylase KDM1A Suppresses the Growth of Multiple Acute Myeloid Leukemia Subtypes.
No sample metadata fields
View SamplesWe sorted CD4 T cells from patients with metastatic melanoma at baseline and after three doses of ipilimumab. Overall design: We examined the differential expression of epigenetic enzymes
Modulation of EZH2 expression in T cells improves efficacy of anti-CTLA-4 therapy.
Specimen part, Subject
View SamplesThis dataset contains microarray data from normal controls (aged 20-99 yrs) and Alzheimer's disease cases, from 4 brain regions: hippocampus, entorhinal cortex, superior frontal cortex, post-central gyrus. Changes in expression of synaptic and immune related genes were analyzed, investigating age-related changes and AD-related changes, and region-specific patterns of change.
Gene expression changes in the course of normal brain aging are sexually dimorphic.
Sex, Subject
View SamplesThis dataset of cognitively normal controls is a subset of the GSE48350 dataset, which additionally contains microarray data from AD brains.
Gene expression changes in the course of normal brain aging are sexually dimorphic.
Sex, Subject
View SamplesHere we report the discovery of highly potent and selective EZH2 small molecule inhibitors, their validation by a cellular thermal shift assay, their application across a large lymphoma cell panel and their efficacy in GCBDLBCL xenograft models. Overall design: RNA-seq of KARPAS-422 cell line RNA, in duplicate, treated with DMSO as control, and EZH2 inhibitors CPI360, EPZ-6438 and GSK126. Eight samples in total.
EZH2 inhibitor efficacy in non-Hodgkin's lymphoma does not require suppression of H3K27 monomethylation.
No sample metadata fields
View SamplesThe goal of this study was to determine if blood circulating monocytes of metastatic breast cancer patient would express a different activation profile compared to healthy donors, in order to use this specific changesas biomarkers to monitor then response to therapy Overall design: CD11b+ cells were extracted from all blood of 4 healthy donors and 4 metastatic breast cancer patients using magnetic beads separation (Miltenyi). CD11b+ cells were then lysed and mRNA was extracted to perform RNASeq.
Bevacizumab specifically decreases elevated levels of circulating KIT+CD11b+ cells and IL-10 in metastatic breast cancer patients.
No sample metadata fields
View SamplesSmoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours.
New insights into the influence of cigarette smoking on urothelial carcinogenesis: smoking-induced gene expression in tumor-free urothelium might discriminate muscle-invasive from nonmuscle-invasive urothelial bladder cancer.
Specimen part, Disease
View SamplesThe goal of this study was to assess whether the presence of HLA-B*35 contributes to activation of ER stress/UPR and inflammation in lcSScPAH PBMC.
The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.
Specimen part
View SamplesCanonical IKK/NF-B signaling is a master regulator of inflammation and innate immunity and has been implicated in the pathogenesis of T1D. To investigate the impact of NF-B activation on -cell homeostasis and diabetes development, we generated a transgenic gain-of-function mouse model allowing conditional NF-B activation via expression of IKK2-CA (constitutively active IKK2 allele) in -cells using the tetracycline-regulated gene expression system. Pdx-1-tTA (knockin model generating Pdx-1 haploinsufficiency) driver mice were used for -cell specific transgene expression. Double transgenic IKK2-CA-pdx-1 mice develop a full-blown immune-mediated diabetes.To identify gene expression changes underlying this diabetes development pancreatic islets of diabetic IKK2-CA-Pdx-1, PDX-1 +/- and control mice were prepared and isolated total RNA was used for microarray analysis.
Long-term IKK2/NF-κB signaling in pancreatic β-cells induces immune-mediated diabetes.
Specimen part
View SamplesTransgenic (Tg) mice expressing nuclear or cytoplasmic human TDP-43 were generated.
Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in mice.
Sex
View Samples