This SuperSeries is composed of the SubSeries listed below.
Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytes.
Specimen part
View SamplesThe oral cavity is the persistent reservoir for EBV with lifelong infection of resident epithelial and B cells. Infection of these cell types results in distinct EBV gene expression patterns that are regulated by epigenetic modifications involving DNA methylation and chromatin structure. Such regulation of EBV gene expression relies on viral manipulation of the host epigenetic machinery that may inadvertently result in long-lasting, oncogenic host epigenetic reprogramming. To test this hypothesis in the context of EBV infection of epithelial cells, we established a transient infection model to identify the epigenetic consequences after EBV infection of immortalized normal oral keratinocytes and subsequent viral loss.
Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytes.
Specimen part
View SamplesEpstein-Barr virus(EBV) is associated with malignancies from lymphoid and epithelial origin. In many cases, an incomplete EBV association is noted and confoundswhate role the virus plays in oncogenesis. A number of viral proteins have been shown to interact with epigenetic factors to regulate both viral and host gene expression. Thus, we hypothesize that EBV may inadvertantly induce epigenetic alterations to the host genome that are maintained upon loss of the virus. If proven, these results would broaden EBV's role in tumorigenesis and provide a mechanism for how a tumor virus can act in a "hit-and-run" fashion.
No associated publication
Specimen part, Cell line
View SamplesTransition of Akata Burkitt lymphoma (BL) cells from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) genomes in vitro is evidence for a viral contribution to tumor maintenance despite the tightly restricted pattern of EBV gene expression in BL. Akata cells retaining virus manifest increased resistance to apoptosis under growth limiting conditions, although ambiguity exists regarding the exact mechanisms involved. By examining global cellular gene expression differences in Akata subclones that had either retained or lost EBV, we identified spermidine/spermine N1-acetyltransferase (SSAT), an inducible acetylating enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes up-regulated upon loss of EBV.
No associated publication
Disease, Disease stage, Treatment
View SamplesTemporal genome profiling of DSS colitis
Temporal genomewide expression profiling of DSS colitis reveals novel inflammatory and angiogenesis genes similar to ulcerative colitis.
No sample metadata fields
View SamplesTemporal geneome profiling of T cell transfer colitis model
Temporal genome expression profile analysis during t-cell-mediated colitis: identification of novel targets and pathways.
Specimen part, Treatment, Time
View SamplesThe activation of TLR-MyD88 (Toll like receptor- Myeloid differentiation factor 88) signaling within T cells functions as a potent costimulatory signal that boosts antitumor and antiviral responses. However, the molecular mechanisms underlying the costimulatory processes are poorly understood. We compared microarray gene analysis data between TLR1-TLR2 stimulated and unstimulated T cell receptor transgenic pmel and MyD88-/-pmel CD8+ T cells and identified changes in the expression levels of several TNF family members. In particular, TLR-stimulation increased 4-1BB levels in pmel but not in MyD88-/-pmel T cells. A link between 4-1BB and TLR1-TLR2 signaling in CD8+ T cells was highlighted by in fact that 4-1BB-/- T cells exhibited suboptimal responses to TLR1-TLR2 agonist, but responded normally to CD28 or OX40 costimulation. Moreover, blocking 4-1BB signaling with antibodies also hindered the costimulatory effects of the TLR1-TLR2 agonist. The elevated levels of 4-1BB transcripts in TLR1-TLR2stimulated cells were not due to increased mRNA stability nor increased histone activation but instead were associated with increased binding of p65 and c-Jun to two distinct 4-1BB promoter sites. Combining TLR1-TLR2 ligand with an agonistic anti-4-1BB antibody enhanced the antitumor activity in mice with established melanoma tumors. These studies reveal that the costimulatory effects of TLR1-TLR2 signaling in CD8+ T cells are in part mediated by 4-1BB and are important for mounting an effective antitumor immune response.
Cross-talk between 4-1BB and TLR1-TLR2 Signaling in CD8+ T Cells Regulates TLR2's Costimulatory Effects.
Specimen part
View SamplesTo examine the effect of wtAPE1 and ubiquitin-APE1 fusion proteins on global gene expression. Total RNA from HEK293 derivatives that express vector alone (ctl), wt-APE1, or ubiquitin-APE1 fusion in the presence of doxycycline were analyzed.
No associated publication
Specimen part, Cell line, Treatment
View SamplesWe have identified genes that are differentially expressed between the bladders of UPII-SV40Tag mice and their age-matched wild-type littermates at 3, 6, 20, and 30 weeks of age. These are ages that correspond to premalignant, carcinoma in situ, and early-stage and later stage invasive UCC, respectively
Identification of genes correlated with early-stage bladder cancer progression.
Specimen part
View SamplesGenes upregulated in stroke infiltrating stem cells were compared against the parent non-infiltrated mouse stem cell line derived from immortomouseTM.
No associated publication
No sample metadata fields
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