Gene Expression patterns in mouse B16-OVA melanoma tumors
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ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE27355 | GEO | 2011/02/17
SECONDARY ACCESSION(S): PRJNA137041
REPOSITORIES: GEO
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Project description:This laboratory focuses on selectin mediated recruitment during adoptive immunotherapy for metastatic cancer. This study seeks to determine changes in the expression levels of Fucosyltransferases, Selectins, and cytokines in normal and inflamed mouse skin, melanoma tumor tissue of different sizes, and tumor cells grown in culture. Since the ability to treat the tumor effectively is directly related to the size of the tumor, differences in glyco-expression patterns may be of interest. In this study, five groups were hybridized and analyzed using the GLYCOv2 array. Each group was analyzed in triplicate. The groups were: Normal mouse skin, normal mouse skin inflamed by treatment with Oxazolone, B16-OVA melanoma tissue from 6 day tumors, B16-OVA melanoma tissue from 11 day tumors, and B16-OVA grown in cell culture.
2011-02-17 | E-GEOD-27355 | biostudies-arrayexpress
Project description:Tumor cell extravasation takes place, similar to leukocytes, in a multi-step process by which cells emigrate from the blood stream through the vascular endothelium into the tissue. Selectins are regarded as the most important molecules for the first capturing step of the cascade. Whether all tumor cells employ selectin dependent adhesion to metastasize or there is an alternative mechanism still is an open question. Comparative transcriptomic analysis of OVCAR8 and SKOV3 cultured cells and revealed that one third of genes encoding proteins involved in the selectin dependent leukocyte like adhesion cascade show lower expression levels in OVCAR8 cultured cells in comparison to that in SKOV3 cultured cells. In contrast to SKOV3 cells, c-Fos overexpression in OVCAR8 cells does not significantly influence expression of the leukocyte like adhesion cascade genes leaving them at similar levels as in control OVCAR8 cells. The intraperitoneal xenograft model of OVCAR8 cells demonstrated that aggressiveness of OVCAR8-derived tumors is not dependent of c-Fos expression level and comparable with that for SKOV3 control tumors. Based on transcriptome array data we analyzed in details expression of genes encoding proteins involved in the leukocyte like adhesion cascade, E- and P-selectin ligands, as well as glycosylation enzymes in both type of tumors. Our results suggest that selectin-dependent mechanism is not the only for adhesion of OVCAR8 ovarian cancer cells. There is at least one additional mechanism of extravasation that does not rely on selectins.
2017-03-31 | GSE97226 | GEO
Project description:Whole Genome Sequencing of the murine breast cancer cell line 4T1 and of the murine melanoma cell line B16-ova was carried out with the aim of identifying somatic mutations. We also ran deep Mass Spectrometry proteomics analysis on the same cell lines, aiming to determine which somatic mutations carry over to the protein expression level. Further, we tested these cancer specific protein epitopes (putative neoantigens) for immunogenicity using mouse models. Finally, the putative neoantigens that showed good immunogenic potential were used in tumor growth control experiments with mice engrafted with the two tumor cell lines. In these experiments we tested whether cancer vaccines based on individual neoantigen peptides (MHC-I) restricted the growth of the tumor compared to adequate controls. The overall aim of the project is to validate the ability of our multi-omics/bioinformatics pipeline to identify and deliver neoantigens that can be used to suppress tumor growth. File names Sample names P10859_101_S1_L001_R1_001_BHKWV3CCXY 4T1_S1_L001_R1_001_BHKWV3CCXY P10859_101_S1_L001_R2_001_BHKWV3CCXY 4T1_S1_L001_R2_001_BHKWV3CCXY P10859_101_S1_L002_R1_001_BHKWV3CCXY 4T1_S1_L002_R1_001_BHKWV3CCXY P10859_101_S1_L002_R2_001_BHKWV3CCXY 4T1_S1_L002_R2_001_BHKWV3CCXY P10859_102_S2_L003_R1_001_BHKWV3CCXY B16-OVA_S2_L003_R1_001_BHKWV3CCXY P10859_102_S2_L003_R2_001_BHKWV3CCXY B16-OVA_S2_L003_R2_001_BHKWV3CCXY P10859_102_S2_L004_R1_001_BHKWV3CCXY B16-OVA_S2_L004_R1_001_BHKWV3CCXY P10859_102_S2_L004_R2_001_BHKWV3CCXY B16-OVA_S2_L004_R2_001_BHKWV3CCXY
2024-01-31 | E-MTAB-13635 | biostudies-arrayexpress
Project description:This laboratory studies 1) enzymes which are involved in selectin ligand formation in leukocytes, 2) how expression of those enzymes is controlled, and 3) basic cell biology of FucT-VII. B cells vs. plasma cells. Study of primary IgG plasma cells. Plasma cells constitute the final stage of B-cell differentiation, and their migration from the lymph nodes and spleen to bone marrow is thought to be an important step in the maintenance of a long-term antibody response to a pathogen. Dr. Kansas has purified primary IgG plasma cells from E-selectin/P-selectin double knockout mice by a negative selection technique and compared their gene expression profile to that of murine B cells using Affymetrix murine oligonucleotide microarray analysis. Highly distinct gene expression profiles were revealed (see Underhill GH et al, Blood. 2003;101:4013-4021). As a follow-up to that experiment, the same probes (in triplicate) derived from primary murine IgG plasma cells and normal B cells were used to probe Glyco-gene Chips. As a follow-up to that experiment, the same probes (in triplicate) derived from primary murine IgG plasma cells and normal B cells were used to probe Glyco-gene Chips.
2011-01-07 | E-GEOD-26480 | biostudies-arrayexpress
Project description:Poly I:C is a powerful immune adjuvant as a result of its agonist activities on TLR-3, MDA5 and RIG-I. Intratumoral administration is conceivably safer than systemic delivery and allows concentrate proinflammatory adjuvanticity in the tumor microenvironment and tumor-draining lymphoid tissue. BO-112 is a nanoplexed formulation of Poly I:C complexed with polyethylenimine that causes tumor cell apoptosis showing immunogenic cell death features and that upon intratumoral release results in more prominent tumor infiltration by T lymphocytes. Intratumoral treatment of subcutaneous tumors derived from MC38, 4T1 and B16F10 with BO-112 leads to remarkable local disease control mediated by CD8+ T lymphocytes, as concluded from selective depletion experiments. Some degree of control of non-injected tumor lesions upon BO-112 intratumoral treatment was found in mice bearing bilateral B16OVA melanomas, that was enhanced when co-treated with systemic anti-CD137 and anti-PD-L1 immunomodulatory mAbs. More abundant CD8+ T lymphocytes were found in tumor-draining lymph nodes and in the tumor microenvironment following intratumoral treatment with BO-112. Enhanced numbers of tumor-specific CTLs recognizing melanosomal antigens and ovalbumin were readily detected among them. Genome-wide transcriptome analyses of injected tumor lesions were consistent with a marked upregulation of the type-I interferon pathway. Intratumorally delivered BO-112 is being tested in cancer patients (NCT02828098) and our results in mice suggest prominent anti-tumor local control through its proimmune effects. To compare the in-vitro and in vivo transcriptional profile induced by BO-112, B16-OVA cell lines were incubated with BO-112 for 24h. BO-112 induces a specific transcriptional profile in B16-OVA cell cultures. Key immunoregulatory genes were found to be differentially expressed between BO-112 and Vehicle-incubated B16-OVA cells.
2019-05-15 | GSE116075 | GEO
Project description:This laboratory works on selectins and their carbohydrate ligands in lymphocyte homing and inflammation. The lab also studies heparin-degrading endosulfatases and their roles in regulating the interactions of growth factors and morphogens with proteoglycans. Gene expression profiles from null and doubly null mice for 2 sulfotransferases (HED-GlcNAc6ST and GlcNAc6ST-1) will be compared to WT mice to find impact on L-selectin ligand formation in lymph nodes. RNA was isolated from the lymph nodes of the 2 types of null mice, 1 type of double null mice, and 1 of wild type mice. 3 duplicates of each strain were analyzed by gene expression profiling. We have null mice and doubly null in two sulfotransferases (HEC-GlcNAc6T and GlcNAc6ST-1) involved in L-selectin ligand formation in lymph nodes. Our functional analysis reveal partial loss (50 and 25%)of lymph node L-selectin ligands in the singly null mice and an 80%loss in the double null mice. We want to identify candidates for the protein scaffolds and underlying posttranslational modifications responsible for the residual L-selectin ligand activity in these mice. We will perform a glycochip analysis with mRNA isolated from lymph nodes of the 3 types of null mice and wild-type mice, all on the C57BL/6 background. Three duplicates from each strain are analyzed, requiring a total of 12 chips. The mice are 8-10 weeks of age and all female.
2011-02-04 | E-GEOD-27056 | biostudies-arrayexpress
Project description: Not available
| S-EPMC6933081 | biostudies-literature
Project description:We want to characterize the glycan moieties on the surface of leukocytes treated with fluorinated analogs of glucosamine. Since these metabolic inhibitors compete with natural-occuring glucosamine used in oligosaccharide chain formation, these compounds have been shown to be effective in lowering Type 2 lactosamine and sialylated Lewis antigens, which results in altered selectin ligand functions. We need to establish specific structural evidence that glycans are indeed blunted/altered. Current research efforts include investigations on how circulating leukocytes traffic to inflamed tissues, how circulating solid tumor cells interact with endothelial linings to enhance metastatic potential, and how treatment with analogs of glucosamine disrupt leukocyte trafficking mechanisms and/or influence effector/regulatory function of T cells.
2011-10-02 | E-GEOD-32556 | biostudies-arrayexpress
Project description:In a previous study by our group, it could be shown that peritoneal selectins mediate the peritoneal spread of pancreatic ductal adenocarcinoma (PDA). In the absence of selectins, Integrin alpha-V (ITGAV) is upregulated in the remaining tumor spots. To study the relevance of ITGAV for PDA’s progression, a knockdown of ITGAV was generated using a shRNA-mediated approach in two PDA cell lines.
2020-07-31 | GSE153702 | GEO
Project description:This study investigates the transcriptome of ADAM12+ mesenchymal stromal cells (MSCs) in B16-OVA (MO5) melanomas
2023-10-05 | GSE206795 | GEO