An Hodgkin Lymphoma cell line have been treated with an LNA inhibitor for miR-9 or with a scramble LNA to identify miR-9 regulated pathways that could be important for Hodgkin Lymphoma pathogenesis.
Inhibition of miR-9 de-represses HuR and DICER1 and impairs Hodgkin lymphoma tumour outgrowth in vivo.
Cell line, Treatment
View SamplesEpstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role.
Molecular signature of Epstein Barr virus-positive Burkitt lymphoma and post-transplant lymphoproliferative disorder suggest different roles for Epstein Barr virus.
Specimen part, Cell line
View SamplesBurkitt lymphoma is the commonest cancer in children in Africa. We compared the gene expression profiles of African Burkitt lymphoma patients with those of cases presented in Western countries in both immunocompetent (sporadic Burkitt lymphoma) and HIV-infected patients (immunodeficiency associated Burkitt lymphoma).
Gene expression analysis uncovers similarity and differences among Burkitt lymphoma subtypes.
Specimen part
View SamplesHuman infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.
Specimen part, Cell line, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Canonical and atypical E2Fs regulate the mammalian endocycle.
Age, Specimen part
View SamplesTo understand the underlying cause and mechanisms of changes in hepatocyte ploidy upon Albumin-Cre mediated deletion of E2f7&8 and Mx1-Cre mediated deletion of E2f1,2&3, we analysed global gene expression of 6 weeks and 2 months liver tissues.
Canonical and atypical E2Fs regulate the mammalian endocycle.
Age, Specimen part
View SamplesTo understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.
E2f1-3 are critical for myeloid development.
Age, Specimen part
View SamplesEpigenetic mechanisms contribute to deregulated gene expression of hematopoietic progenitors in Myelodysplastic Syndromes (MDS). Hypomethylating agents are able to improve peripheral cytopenias in MDS patients. To identify critical gene expression changes induced by hypomethylating agents, we analyzed gene expression profiling (GEP) of myelodysplastic and normal CD34+ hematopoietic stem cells treated in vitro with or without decitabine. Four MDS and two untreated early stage Hodgkins lymphomas were analyzed for GEP. Mock treated CD34+ stem cells segregate according to diagnosis and karyotype. After decitabine treatment, gene expression changes were more consistent on MDS CD34+ cells with abnormal kayotype. Comparing decitabine-induced genes with those found down-regulated in mock-treated MDS cells, we identified a list of candidate tumor suppressor genes in MDS. By real-time RT-PCR we confirmed expression changes for three selected genes CD9, CXCR4 and GATA2 in 12 MDS patients and 4 controls. CD9 was widely repressed in most MDS CD34+ cell samples, although similar levels of methylation were found in both normal and MDS total bone marrows. CXCR4 promoter methylation was absent in total bone marrows from 36 MDS patients. In conclusion, changes in gene expression changes induced by hypomethylating treatment are more pronounced in CD34+ cells from abnormal karyotype.
Gene expression profiling of myelodysplastic CD34+ hematopoietic stem cells treated in vitro with decitabine.
Sex, Age, Specimen part, Disease
View SamplesTo identify novel Nurr1 target genes we have used microarrays strategies in rat midbrain primary cultures, enriched in dopaminergic neurons, by the action of basic fibroblast growth factor (bFGF, 20ng/ml) and Sonic hedgedog (SHH), following upregulation of Nurr1 expression by depolarization.To this aim we have treated the cultures after 9 days in vitro for 2h with high KCl and collected 30 min or 2 h after the end of depolarization (2h + 30 min or 2h + 2h). With this experimental protocol we have identify a putative Nurr1 regulator and Nurr1 target
Bdnf gene is a downstream target of Nurr1 transcription factor in rat midbrain neurons in vitro.
Specimen part
View SamplesThe following abstract from the submitted manuscript describes the major findings of this work.
A role for peroxisome proliferator-activated receptor γ coactivator-1 in the control of mitochondrial dynamics during postnatal cardiac growth.
Specimen part
View Samples