Gene expression analysis of B16-F1 melanoma tumors established in WT and Stat2KO mice
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ABSTRACT: STAT2 is an essential transcription factor in type I interferon (IFN) signaling. STAT2 mediates the antigrowth and apoptotic effects of IFN as demonstrated in cell lines thus leading to the hypothesis that STAT2 has tumor suppressor function. We used microarrays to identify genes in the tumors that are STAT2 dependent and important in anti-tumor immunity. B16-F1 melanoma tumor cells were implanted on the dorsal flank of either wild type (WT) or Stat2KO (S2KO). Tumor growth was monitored during the course of 3 weeks. S2KO mice developed larger tumors when compared to WT mice.
Project description:STAT2 is an essential transcription factor in type I interferon (IFN) signaling. STAT2 mediates the antigrowth and apoptotic effects of IFN as demonstrated in cell lines thus leading to the hypothesis that STAT2 has tumor suppressor function. We used microarrays to identify genes in the tumors that are STAT2 dependent and important in anti-tumor immunity.
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 Total RNA obtained from tumor microenvironment tissues (at Day 4 and Day 14 after tumor inoculation) compared to control tissues.
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.
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
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.
Project description:extracellular PTEN treatment did not affect the growth of PTEN knockout B16-F10 cells cultured in vitro. , To investigate whether extracellular PTEN act on the tumor microenvironment to exert a tumor-suppressive role in vivo,molecular changes caused by PTEN treatment inside the B16-F10-PTEN tumors were monitored by RNA sequencing.
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.
Project description:Analysis of B16 tumor microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchastrated the immune reponse triggered in presence of tumors
Project description:Histotripsy is a novel focused ultrasound tumor ablation modality with potent immunostimulatory effects. To measure the spatiotemporal kinetics of local and abscopal responses to histotripsy, C57BL/6 mice bearing bilateral flank B16 melanoma or Hepa1-6 hepatocellular carcinoma tumors were treated with unilateral sham or partial histotripsy. Treated and Controltralateral untreated (abscopal) tumors were analyzed using multicolor immunofluorescence, digital spatial profiling, RNA sequencing (RNASeq), and flow cytometry.
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