By using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell lines.
Expression and Regulation of the Endogenous Retrovirus 3 in Hodgkin's Lymphoma Cells.
Cell line
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell line L-428 after knock-down of the tumor antigen PRAME (preferentially expressed antigen in melanoma)
Knock-down of PRAME increases retinoic acid signaling and cytotoxic drug sensitivity of Hodgkin lymphoma cells.
Specimen part, Cell line
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell line L-540 after tretament with the histone deactelyse inhibitor vorinostat.
Histone deacetylase inhibition restores cisplatin sensitivity of Hodgkin's lymphoma cells.
Specimen part, Cell line, Treatment
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile in a panel of germ cell tumour cell lines
Differentiation-Dependent Regulation of Human Endogenous Retrovirus K Sequences and Neighboring Genes in Germ Cell Tumor Cells.
Specimen part, Cell line
View SamplesInducible co-stimulator (ICOS) interaction with its ligand (ICOSL) is involved in several T cell effector functions. While blockade of ICOS:ICOSL interaction in chronic graft versus host disease (GVHD) seems benefi cial, results for acute GVHD remain controversial. To further elucidate its role in acute GVHD, C57BL / 6 mice were lethally irradiated and reconstituted with allogeneic spleen cells in the absence or presence of ICOSL-blocking mAb. Mice reconstituted with allogeneic spleen cells experienced severe GVHD and died untreated within 6 9 days after transplantation. Mice treated with an anti-ICOSL mAb starting from day 3 after transplantation gained weight again and survived for at least additional 12 days, although the treatment was already stopped at day 11 after transplantation. In contrast, the anti-ICOSL treatment starting from day 0 did not prevent GVHD. The diff erence between therapeutic (day 3) and prophylactic (day 0) anti-ICOSL treatment was independent of CD25 + CD4 + regulatory T cells since their depletion did not abrogate the therapeutic eff ect of ICOSL blockade. Microarray analysis revealed IFN- and chemokine up-regulation in spleen cells of prophylactically treated mice, emphasizing kinetic dependence of acute GVHD modulation via blockade of ICOS:ICOSL interaction.
Only therapeutic ICOS:ICOSL blockade alleviates acute graft versus host disease.
Sex, Specimen part
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of SHSY5Y neuroblastoma cells after treatment with cobalt chloride
Investigation of Endogenous Retrovirus Sequences in the Neighborhood of Genes Up-regulated in a Neuroblastoma Model after Treatment with Hypoxia-Mimetic Cobalt Chloride.
Specimen part, Cell line
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of liver biopsies from young and aged donors
Impairment of Host Liver Repopulation by Transplanted Hepatocytes in Aged Rats and the Release by Short-Term Growth Hormone Treatment.
Specimen part
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell line L-428 after knock-down of DUSP5 (dual specificity phosphatase 5)
Expression of dual-specificity phosphatase 5 pseudogene 1 (DUSP5P1) in tumor cells.
Specimen part, Cell line
View SamplesComparison of gene expression profiles between neuroblastoma samples and Ewing family tumor samples. RNA from native tumor samples was processed for DNA-microarray analysis using Affymetrix HG-U133A microarrays. Primary image analysis was performed using MAS 5.0 and data were scaled to an target intesity of 500.
DNA microarrays reveal relationship of Ewing family tumors to both endothelial and fetal neural crest-derived cells and define novel targets.
No sample metadata fields
View SamplesWe found the PRC2 component EZH2 to be upregulated by the pathognomonic fusion oncogene EWS-FLI1 in Ewing tumors and mesenchymal stem cells (Richter GH et al., Proc Natl Acad Sci U S A. 2009;106:5324-9). Downregulation of EZH2 by RNA interference in Ewing tumor cell lines suppressed oncogenic transformation in vitro and in vivo. These data suggest that EZH2 might play a central role in Ewing Tumor pathology.
Epigenetic maintenance of stemness and malignancy in peripheral neuroectodermal tumors by EZH2.
No sample metadata fields
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