Filters
Technology
Platform
GSE149910
Homo sapiens
18 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Aryl hydrocarbon receptor (AHR) activation by tryptophan (Trp) catabolites enhances tumor malignancy and suppresses anti-tumor immunity. Hitherto, indoleamine-2,3-dioxygenase 1 (IDO1) or tryptophan- 2, 3-dioxygenase (TDO2) are recognized as the main Trp-catabolizing enzymes (TCEs) responsible for the generation of AHR agonists. Here, the ability of the aromatic L-amino acid oxidase, interleukin 4 induced 1 (IL4I1), to activate the AHR was investigated using IL4I1 knockout CAS-1 glioblastoma cells.
Publication Title
IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Analysis of the effect of IL4I1 on gene expression of CD8 T-cells in CLL
Publication Title
IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Indole-3-pyruvate (I3P), an endogenous metabolite derived from tryptophan by gut microbiota and IL4I1 enzyme in humans can potentially activate the transcriptional activity of the Aryl Hydrocarbon receptor. Here we test this by stimulating AHR proficient U-87MG cells with I3P alone or in combination with the AHR antagonist SR1.
Publication Title
IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
Description
Cell lines derived from tumor tissues have been used as a valuable system tostudy gene regulation and cancer development. Comprehensive characterization ofthe genetic background of cell lines could provide clues on novel genes responsiblefor carcinogenesis and help in choosing cell lines for particular studies. Here, we havecarried out whole exome and RNA sequencing of commonly used glioblastoma (GBM)cell lines (U87, T98G, LN229, U343, U373 and LN18) to unearth single nucleotidevariations (SNVs), indels, differential gene expression, gene fusions and RNA editingevents. We obtained an average of 41,071 SNVs out of which 1,594 (3.88%) werepotentially cancer-specific. The cell lines showed frequent SNVs and indels in someof the genes that are known to be altered in GBM- EGFR, TP53, PTEN, SPTA1 andNF1. Chromatin modifying genes- ATRX, MLL3, MLL4, SETD2 and SRCAP also showedalterations. While no cell line carried IDH1 mutations, five cell lines showed hTERTpromoter activating mutations with a concomitant increase in hTERT transcript levels.Five significant gene fusions were found of which NUP93-CYB5B was validated. Anaverage of 18,949 RNA editing events was also obtained. Thus we have generated acomprehensive catalogue of genetic alterations for six GBM cell lines.
Publication Title
Elucidating the cancer-specific genetic alteration spectrum of glioblastoma derived cell lines from whole exome and RNA sequencing.
Sample Metadata Fields
No sample metadata fields
View Samples- Arabidopsis thaliana
- 30 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Comparative transcriptomic analysis of Arabidopsis thaliana yda11 plants (in Col-0 background), and wild-type plants (Col-0) non-infected or infected with the necrotrophic fungal pathogen Plectosphaerella cucumerina BMM (PcBMM)
Publication Title
YODA MAP3K kinase regulates plant immune responses conferring broad-spectrum disease resistance.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Mus musculus
- 26 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
While it is clear that T cell derived IFN has to act on tumor stroma cells for rejection of solid tumors, it is not clear which tumor stroma cells are targets. We studied how IFN affects gene expression in tumor blood vessels in vivo. To study the effect on endothelial cells, we either used a model of ectopic IFN (MCA313 tumors) or IFN-GFP fusion protein (J558L tumors) expression in tumors, or we used T cell derived IFN in large vascularized 16.113 tumours. Tumors were grown in mice that were expressing the IFN receptor ubiquitously (J558L tumors + IFN-GFP treatment and 16.113 tumors + T cell treatment) or in some experiments the IFN-receptor was expressed exclusively in endothelial cells (MCA313 tumor + IFN treatment).
Publication Title
Tumour ischaemia by interferon-γ resembles physiological blood vessel regression.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Affymetrix HuGene ST 1.0 microarrays were used to study and compare gene expression in peripheral blood CD8+ T cells of human patients with Acute Infectious Mononucleosis (AIM; acute EBV infection) and during convalescence (CONV; 6-12 months after AIM visit). Blood samples were drawn from ten human patients with AIM and again during their covalescence (CONV). Peripheral blood mononuclear cells were isolated and cryopreserved. Paired AIM and CONV samples were thawed and CD8+ T cells purified with magnetic beads. RNA was isolated and processed for hybridization according to the Affymetrix protocol
Publication Title
A Gene Expression Signature That Correlates with CD8+ T Cell Expansion in Acute EBV Infection.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Homo sapiens
- 33 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Uterine leiomyomata (UL), the most common neoplasm in reproductive-age women, have recurrent cytogenetic abnormalities including del(7)(q22q32). To develop a molecular signature, matched del(7q) and non-del(7q) tumors identified by FISH or karyotyping from 11 women were profiled with expression arrays. Our analysis using paired t-tests demonstrates this matched design is critical to eliminate confounding effects of genotype and environment that underlie patient variation. A gene list ordered by genome-wide significance showed enrichment for the 7q22 target region. Modification of the gene list by weighting each sample for percent of del(7q) cells to account for the mosaic nature of these tumors further enhanced the frequency of 7q22 genes. Pathway analysis revealed two of the 19 significant functional networks were associated with development and the most represented pathway was protein ubiquitination, which can influence tumor development by stabilizing oncoproteins and destabilizing tumor suppressor proteins. Array CGH (aCGH) studies determined the only consistent genomic imbalance was deletion of 9.5 megabases from 7q22-7q31.1. Combining the aCGH data with the del(7q) UL mosacism-weighted expression analysis resulted in a list of genes that are commonly deleted and whose copy number is correlated with significantly decreased expression. These genes include the proliferation inhibitor HPB1, the loss of expression of which has been associated with invasive breast cancer, as well as the mitosis integrity-maintenance tumor suppressor RINT1. This study provides a molecular signature of the del(7q) UL subgroup and will serve as a platform for future studies of tumor pathogenesis.
Publication Title
Identifying the molecular signature of the interstitial deletion 7q subgroup of uterine leiomyomata using a paired analysis.
Sample Metadata Fields
Disease
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Uterine leiomyomata (UL), the most common neoplasm in reproductive age women, have recurrent cytogenetic abnormalities including t(12;14). To develop a molecular signature, matched t(12;14) and non-t(12;14) tumors identified by FISH or karyotyping from each of 9 women were profiled using Affymetrix GeneChip U133 Plus 2.0 oligonucleotide arrays. Model analysis demonstrated the necessity for a matched design to eliminate the confounding effect of genotype and environment that underlay patient to patient variation.
Publication Title
Expression profiling of uterine leiomyomata cytogenetic subgroups reveals distinct signatures in matched myometrium: transcriptional profilingof the t(12;14) and evidence in support of predisposing genetic heterogeneity.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 32 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Ebf1 is a transcription factor with documented, and dose dependent, functions in both normal and malignant B-lymphocyte development. In order to understand more about the role of Ebf1 in malignant transformation, we have investigated the impact of reduced functional Ebf1 dose on early B-cell progenitors. Gene expression analysis in loss and gain of function analysis suggested that Ebf1 was involved in the regulation of genes of importance for DNA repair as well as cell survival. Investigation of the level of DNA damage in steady state as well as after induction of DNA damage by UV light supported that pro-B cells lacking one functional allele of Ebf1 display a reduced ability to repair DNA damage. This was correlated to a reduction in expression of Rad51 and combined analysis of published 4C and chromatin Immuno precipitation data suggested that this gene is a direct target for Ebf1. Even though the lack of one allele of Ebf1 did not result in any dramatic increase of tumor formation, we noted a dramatic increase in the formation of pro-B cell leukemia in mice carrying a combined heterozygote mutation in the Ebf1 and Pax5 genes. Even though the tumors were phenotypically similar and stable, we noted a large degree of molecular heterogeneity well in line with a mechanism involving impaired DNA repair. Our data support the idea that Ebf1 controls homologous DNA repair in a dose dependent manner and that this may explain the frequent involvement of Ebf1 in human leukemia
Publication Title
Ebf1 heterozygosity results in increased DNA damage in pro-B cells and their synergistic transformation by Pax5 haploinsufficiency.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples