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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Analysis of tumour gene expression from fibrosarcoma mouse model following Treg depletion

ABSTRACT: Experiment was designed to look at the differences in gene expression between mice which responded to Treg depletion and began to control tumour growth, mice which could not bring tumour growth under control, untreated mice and a lymp node comparison.

ORGANISM(S): Mus musculus

SUBMITTER: Alex Greenshields-Watson

PROVIDER: E-MTAB-9351 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression changes during resistance toward vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy in renal cell carcinoma (RCC)

Project description:This study was performed to understand the gene expression changes that accompany treatment of renal cell carcinoma (RCC) with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy. Human RCC cell lines were implanted into the flanks of nude beige mice, allowed to reach 12mm in long axis, and then treated with TKIs (sunitinib or sorafenib). Tumors were excised at 2 timepoints (prior to any therapy and at the 20mm endpoint of the study) and gene expression analysis was performed. Sunitinb or sorafenib were administered to mice bearing either 786-O or A498 xenografts. Mice were sacrificed and tumors excised for RNA extraction at pretreatment size of 12mm, or at 20mm, the mandated maximum tumor size allowed at our institution.

2015-05-21 | E-GEOD-64052 | biostudies-arrayexpress

Transcription profiling of human A549 induced tumours in mice treated with PCI-5002, PCI-5003, or control vehicle

Project description:We have demonstrated that water-soluble zinc ionophores can be administered to mice at relatively high doses and inhibit the growth of A549 lung cancer cells grown in xenograft models. Gene expression profiles of tumor specimens harvested from mice four hours after treatment confirmed that the activation of stress responsive genes occurs in vivo. These findings lead us to propose that the pharmacologic delivery of zinc to tumors using water solubilized ionophores is a potential approach to cancer therapy. Experiment Overall Design: 1.25 million A549 cells were injected subcutaneously/intramuscularly into the right hind flank of 6 week old CD-1 nude mice that had been irradiated with 4 Gy of total body irradiation from a 137Cs radiation source one day prior to tumor implantation. When the average size of tumors reached approximately 100 mm3, mice were randomized by tumor size to treatment groups, typically containing 6-8 mice per group. Tumor and body weight measurements were performed three times per week. Tumor volume was calculated using the equation V (mm3) = a x b2/2, where a is the largest diameter and b is the smallest diameter. No significant body weight loss was observed. To perform gene expression profiling, mice were treated intravenously with one dose (100 Î¼mol/kg) PCI-5002, PCI-5003, or control vehicle (4 mice per group) when the average A549 tumor size reached 500 mm3. After four hours, tumors were harvested and snap frozen immediately on dry ice. Tumor tissue was homogenized, and total RNA was isolated and subjected to analysis using Human Genome U133 Plus 2.0 Arrays as described above.

2008-06-15 | E-GEOD-6962 | biostudies-arrayexpress

Transcription profiling of human samples - synthesis and anticancer properties of water-soluble Zinc ionophore: cell culture and xenograft model (GEO Super Series)

Project description:This SuperSeries is composed of the following subset Series:; GSE6960: Synthesis and Anticancer Properties of Water-Soluble Zinc Ionophores 1; GSE6962: Synthesis and Anticancer Properties of Water-Soluble Zinc Ionophores 2 Experiment Overall Design: Refer to individual Series

2008-06-15 | E-GEOD-6972 | biostudies-arrayexpress

The Id-RAP1 axis is essential for glioma maintenance and residency of glioma cells in the perivascular niche

Project description:The experiment was designed to achieve Cre recombinase mediated deletion of Id1, Id2 and Id3 in a temporally controlled fashion in tumor cells of Id1, Id2, Id3 floxed mice with the aim of comparing the gene expression profiles of Id expressing versus Id deleted tumors.

2013-04-30 | E-MTAB-1303 | biostudies-arrayexpress

Transcription profiling of nude mice tumor biopsies generated by the injection of mesenchymal stem cells (MSC)

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2006-12-26 | E-MEXP-562 | biostudies-arrayexpress

Transcription profiling of human A549 lung cancer cells and their isogenic mitochondrial DNA (mtDNA)-depleted rho zero counterparts grown in cell culture and as tumor xenografts in immune-deficient mice.

Project description:Interactions between the gene products encoded by the mitochondrial and nuclear genomes play critical roles in normal eukaryotic cellular function. Here, we characterized the metabolic and transcriptional properties of A549 lung cancer cells and their isogenic mitochondrial DNA (mtDNA)-depleted rho zero counterparts grown in cell culture and as tumor xenografts in immune-deficient mice. A manuscript summarizing our conclusions is under review. Experiment Overall Design: A549 rho zero and their parental A549 cells were grown in culture and as xenografts in nude mice. All experiments conducted in culture were performed in triplicate (6 experiments total) and all experiments conducted in xenografts were performed in quadruplicate (8 experiments total). A manuscript summarizing our experimental design is under review.

2008-06-11 | E-GEOD-10957 | biostudies-arrayexpress

miR-125b: A Rheostat of Growth versus Stress-Induced MAPKs That Governs Stemness and OncomiR Addiction in Skin

Project description:We analyze the globel gene expression changes in the tumor initiating cells of regressing miR-125b addicted tumors after oncomiR withdrawal For Histone-H2BGFP expression in DTG tumor cells, the U6 promoter was deleted in the PLKO-PGK-H2B-GFP vector throughNdeI-AgeI digestion, Quick Blunting Kit treatment (NEB), and self-ligation. The resulting PLNA-PGK-H2BGFP plasmid was packaged into lentivirus and used to infect ~1x106freshly sorted α6hiβ1hi DTG tumor cells. After 30 min, cells were then extensively washed and immediately engrafted onto backskins of Nude mice by intradermal transplantation. GFP+α6hiβ1hicells were FACS-isolated from resulting tumors and then serially transplanted as above. For RNA seq analysis of the miR-125b addicted tumor regression process, H2BGFP labeled DTG tumor cells were intradermally engrafted onto backskins of Nude mice (1x104cells/site). Tumors were allowed to grow to ~1cm diameter. Mice were then taken Off Dox by transferring them to regular food for 0, 4, 7 days. GFP+α6hiβ1hiwere then FACS-isolated from the tumors. Two or three independent replicates were collected for each time point. Total RNAswere extracted from the FACS-sorted cells using the miRNeasy Mini Kit (Qiagen) according to the vender’s protocol. Expression of miR-125b in each sample was quantified by RT-PCR using TaqMan MicroRNA Assays (Applied Biosystems). For RNA seq, RNA samples were submitted to the Genomics Resources Core Facility of the Weill Cornell Medical College for library construction using IlluminaTruSeq Stranded mRNA Sample Prep Kit and then sequencing using Illumina HiSeq2000. Resultswere analyzed via the Galaxy web platform using TopHat for initiate mapping and Cufflinks for transcripts assembling and expression level estimation (Computing FPKM: fragments per kilobase of exon per million fragments mapped). The MM9 genome assembly (UCSC Genome Browser) was used as reference genome for all analyses. Low expression genes

2014-02-12 | E-GEOD-54704 | biostudies-arrayexpress

Mouse liver macrophage gene expression following hepatic fibrosis

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2011-07-01 | E-MEXP-3177 | biostudies-arrayexpress

Gene expression profiling of oncogenic NRAS driven mouse melanomas that have developed resistance to NRAS withdrawal

Project description:Targeted therapies have the potential to revolutionize cancer care by providing personalized treatment strategies that are less toxic and more effective but it is clear that for most solid tumors suppression of a single target is not sufficient to prevent development of resistance. A powerful method to identify mechanisms of resistance and targets for combination therapy is to use an in vivo genetic approach. We have developed a novel retroviral gene delivery mouse model of melanoma that permits control of gene expression post-delivery using the tetracycline (tet)-regulated system. In this study we used this melanoma model to select for resistant tumors following genetic inhibition of mutant NRAS. Analysis of tumors that became resistant to NRAS suppression revealed that the most common mechanism of resistance was overexpression of the Met receptor tyrosine kinase (RTK). Importantly, inhibition of Met overcomes NRAS resistance in this context. Analysis of NRAS mutant human melanoma cells revealed that inhibition of MEK is also associated with adaptive RTK signaling. Furthermore, co-inhibition of RTK signaling and MEK overcomes acquired MEK inhibitor resistance in NRAS mutant melanoma. These data suggest that combined inhibition of RTK and MEK signaling is a rational therapeutic strategy in mutant NRAS driven melanoma. Reversible NRAS Q61R expression in the melanocytes of DCT-TVA;Ink4a/Arf lox/lox mice (FVB/n) was achieved by transducing the animals with Tet-off and TRE-NRASQ61R-IRES-Cre avian leukosis viruses. After tumor initiation, the expression of NRAS Q61R was turned off by administrating doxycycline. Despite initial regression, tumors in 40% of mice developed resistance to NRAS Q61R withdraw. Seven resistant tumors and one control tumor where NRAS Q61R expression was not interrupted were subjected to genome-wide gene expression profiling.

2014-10-31 | E-GEOD-51906 | biostudies-arrayexpress

Transcription profiling by array of miRNA in mouse models of melanoma comparing niches of tumour tissue to adjacent normal tissue

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