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Systems analysis of B16-WT, B16-shTGFb and B16-shVEGF tumor microenvironment 4 or 14 days after tumor inoculation

ABSTRACT: Analysis of B16 tumor microenvironments at gene expression level. The hypothesis tested in the present study was that Tregs orchastrated the immune reponse triggered in presence of tumors Total RNA obtained from tumor microenvironment tissues (at Day 4 and Day 14 after tumor inoculation) compared to control tissues.

ORGANISM(S): Mus musculus

SUBMITTER: Djamel NEHAR-BELAID

PROVIDER: E-GEOD-73384 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Systems analysis of B16-WT, B16-shTGFb and B16-shVEGF tumor microenvironment 4 or 14 days after tumor inoculation

Project description:Analysis of B16 tumor microenvironments at gene expression level. The hypothesis tested in the present study was that Tregs orchastrated the immune reponse triggered in presence of tumors

2016-09-01 | GSE73384 | GEO

Systems analysis of B16 tumor microenvironment 4 or 14 days after tumor inoculation

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Whole transcriptomic analysis of B16 tumor environment 14 days after tumor inoculation in the absence of regulatory T cells (Treg)

Project description:Analysis of weakly immunogenic, B16 tumor environment at gene expression level after Treg depletion

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Comprehensive analysis of pathological changes in tumor of B16 with CCND1 overexpression

Project description:Aims: CCND1 amplification was an unfavorable prognostic factor for patients with melanoma. This study aimed to investigate the molecular changes in tumor of B16 with CCND1 overexpression. Methods: High-throughput sequencing was used to identify genes that were differentially expressed in tumor between B16 controls and B16 with CCND1 overexpression. Tumors of B16 Ctrl (n=3) and B16 with CCND1 overexpression (n=3) were enrolled in this study. Results: mRNA expression of genes associated with immunity, such as CD8, Gzm, B2m, and Tap1 were decreased in tumors with CCND1 overexpression. Conclusion: CCND1 overexpression is associated with an immunosuppressive microenvironment.

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Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated B16 tumors edited with control or TBK1-targeting sgRNAs.

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proteome analysis of Lung tissue of mice bearing B16-F10-luc-G5 melanoma tumor with sleep fragmentation and with or with out the asdmistration of GL-pp

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2021-09-10 | PXD025171 | Pride

RNA sequencing analysis of B16-F1, B16-F1R2 and B16-F1R2L

Project description:We wanted to correlate the protein cargo of secreted exosomes with gene expression pattern in B16-F1 and B16-F1R2. For that purpose, we performed RNA sequencing analysis of B16-F1, B16-F1R2 and B16-F1R2L (Fig.1E). We identified >3000 genes significantly up-regulated and >1000 significantly down-regulated in B16-F1R2 model compared to B16-F1, using a false discovery rate (FDR) of 0.05.

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Systems analysis of uterine microenvironment in Treg depleted pregnant mice at 12 days after fertilization

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WGS for B16-OVA and 4T1 murine cancer cell lines

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

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Gene Expression patterns in mouse B16-OVA melanoma tumors

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