The aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors after treatment with hydroxytyrosol (a natural compound from virgin olive oil). To this end, a cDNA microarray experiment was performed (Affymetrixs Rat Genome 230 2.0 array). This gene expression study was carried out on the tumor biopsy samples prior to hydroxytyrosol treatment, and compared with matched tumor biopsy samples after completion of the hydroxytyrosol treatment schedule. The result of this study was the identification of several genes related to apoptosis, cell cycle arrest, proliferation, differentiation, survival and transformation-related genes.
Hydroxytyrosol inhibits growth and cell proliferation and promotes high expression of sfrp4 in rat mammary tumours.
Sex, Age, Specimen part, Treatment
View SamplesThe aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors after treatment with adriamycin. To this end, a cDNA microarray was performed (Affymetrixs Rat Genome 230 2.0 array). This gene expression study was carried out on the tumor biopsy samples prior to adriamycin treatment, and compared with matched tumor biopsy samples after completion of the adriamycin treatment schedule.
Hydroxytyrosol inhibits growth and cell proliferation and promotes high expression of sfrp4 in rat mammary tumours.
Sex, Age, Specimen part, Treatment
View SamplesThe aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors from an initial stage to the moment of sacrifice. To this end, a cDNA microarray was performed (Affymetrixs Rat Genome 230 2.0 array). This gene expression study was carried out on the umor biopsy samples and compared with matched tumor biopsy samples once the study ended (7 weeks after initial biopsy).
Hydroxytyrosol inhibits growth and cell proliferation and promotes high expression of sfrp4 in rat mammary tumours.
Sex, Age, Specimen part, Treatment
View SamplesGlioblastomas (GBM) are one of the most frequent and aggressive brain tumors. In these malignancies, progesterone (P4) promotes proliferation, migration, and invasion. The P4 metabolite allopregnanolone (3-THP) similarly promotes cell proliferation in the U87 human GBM cell line.
Allopregnanolone Alters the Gene Expression Profile of Human Glioblastoma Cells.
Specimen part, Cell line, Treatment
View SamplesHow artificial environmental cues are biologically integrated and transgenerationally inherited is still poorly understood. Here, we investigate the mechanisms of inheritance of reproductive outcomes elicited by the model environmental chemical Bisphenol A (BPA) in C. elegans. We show that BPA exposure causes the derepression of an epigenetically silenced transgene in the germline for 5 generations, regardless of ancestral response. ChIP-seq, histone modifications quantitation, and immunofluorescence assays revealed that this effect is associated with a reduction of the repressive marks H3K9me3 and H3K27me3 in whole worms and in germline nuclei in the F3 as well as with reproductive dysfunctions including germline apoptosis and embryonic lethality. Furthermore, targeting of the Jumonji demethylases JMJD-2 and JMJD-3/UTX-1 restores H3K9me3 and H3K27me3 levels, respectively, and fully alleviates the BPA-induced transgenerational effects. Together, our results demonstrate the central role of repressive histone modifications in the inheritance of reproductive defects elicited by a common environmental chemical exposure. Overall design: First generation C. elegans were exposed to either water, DMSO or BPA for for 48 hours, third generation (F3) worms were used for RNA-seq experiments.Total RNA was extracted from needle-dissected gonads of F3 adult worms in 4 replicates of H2O, DMSO, and BPA-exposed P0 nematodes.
The Memory of Environmental Chemical Exposure in C. elegans Is Dependent on the Jumonji Demethylases jmjd-2 and jmjd-3/utx-1.
Treatment, Subject
View SamplesIn this data, we examined Transcriptome detection and expression in 8 samples of Retinoblastoma. We found a central core shared by all samples .
Discovery of a transcriptomic core of genes shared in 8 primary retinoblastoma with a novel detection score analysis.
Disease
View SamplesTo investigate the differences of expression patterns in primary chicken embryo fibroblasts (CEFs) under conditions of contact-inhibition and serum starvation, we undertook a gene profiling study to characterize the transcriptomes of CEFs grown under conditions of contact inhibition, serum starvation or both, in relation to normal growing (cycling) cells.
Extracellular Signal-Regulated Kinase 2 and CHOP Restrict the Expression of the Growth Arrest-Specific p20K Lipocalin Gene to G0.
Specimen part
View SamplesThe bone marrow microenvironment is composed of heterogeneous cell populations of non-hematopoietic cells with complex phenotypes and undefined trajectories of maturation. Among them, mesenchymal cells maintain the production of stromal, bone, fat and cartilage cells. Resolving these unique cellular subsets within the bone marrow remains challenging. Here, we used single-cell RNA-sequencing of non-hematopoietic bone marrow cells to define specific subpopulations. Furthermore, by combining computational prediction of the cell state hierarchy with known expression of key transcription factors, we mapped differentiation paths to the osteocyte, chondrocyte, and adipocyte lineages. Finally, we validated our findings using lineage-specific reporter strains and targeted knockdowns. Our analysis reveals differentiation hierarchies for maturing stromal cells, determines key transcription factors along these trajectories, and provides an understanding of the complexity of the bone marrow microenvironment. Overall design: Single-cell mRNA sequencing of stromal cells from mouse bone marrow. Sample Stroma1 represents 948 final filtered single cells. Sample Stroma2 represents 1899 final filtered single cells.
Mapping Distinct Bone Marrow Niche Populations and Their Differentiation Paths.
Specimen part, Cell line, Subject
View SamplesObesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam celllike cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization.
Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice.
Specimen part
View SamplesMantle cell lymphoma (MCL) is an aggressive neoplasm with poor outcome. However, some patients have an indolent disease (iMCL) and may not require intensive treatment at initial diagnosis. Diagnostic criteria to recognize these patients are not available. We hypothesized that the analysis of the genetic and expression features of the tumors may help to identify patients with an indolent clinical evolution and provide biomarkers that could be used in the clinical setting.
Genomic and gene expression profiling defines indolent forms of mantle cell lymphoma.
Disease, Disease stage
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