Project description:To investigate how tumor cells respond to alisertib and navitoclax single agents and combonation therapy in vivo, mice with melanoma were treated with these agents or vehicle-contol. RNAseq was used to investigate gene expression in tumors
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:B16 melanoma cells were screened with a CRISPR library against TSGs in vitro and as tumors in Rag1-null and immunocompetent WT C57BL/6 mice
Project description:This SuperSeries is composed of the following subset Series: GSE11580: Time course RA-treatment of B16 mouse melanoma cells GSE11584: Melan-a mouse melanocytes vs. B16 mouse melanoma cells Keywords: SuperSeries Refer to individual Series
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. 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:Tumor resistance to anti-cancer drugs is a major huddle in chemotherapy. To identify cancer genes that contribute to chemoresistance, B16 mouse melanoma cells were used as a model. We used microarrays to decipher the specific gene regulation in doxorubicine treated B16 mouse melanoma cells. Keywords: Time course
Project description:On day 7 after B16 melanoma cells transplantation, C57Bl6 mice with subcutaneous palpable tumors were randomly divided into 2 groups for experimental treatment with Dacarbazine. Group 1 «Control (PBS) », n=5, animals in this group were intraperitoneally injected with phosphate buffered saline in a volume of 250 µl. Group 2 «DTIC», n=5, animals in this group were intraperitoneally injected with a solution of Dacarbazine (DTIC) (Sigma-Aldrich, USA) in phosphate buffer at a concentration of 50 mg/kg of animal weight. Injections with PBS or DTIC were carried out three times on days 8, 10 and 12 after melanoma cell transplantation, on day 14, mice were sacrificed for further analysis of primary tumors and organs.
Project description:Gene expression signature of Treg cells in B16 melanoma was measured and compared to B16-infiltrating CD4+ Tconv cells and CD8+ T cells as well as splenic Treg cells, CD4+ Tconv cells and CD8+ T cells.
Project description:CD8 T cells are the main effectors of the adaptive immune response against intracellular pathogens and cancer. Chronic antigen stimulation and inflammation lead to CD8 T cell differentiation and function that differ from those generated during acute infections. A comprehensive definition of the heterogeneity existing within both tumor-specific and total CD8 tumor-infiltrating T cells remains to be clearly established. To investigate this heterogeneity at the transcriptomic level, we performed paired single-cell RNA and TCR sequencing of >3500 CD8 T cells infiltrating B16 murine melanoma tumors, including cells of known tumor-specificity.
Project description:Hypoxia-driven alterations in the B16 melanoma cell transcriptome account for a higher metastatic potential: evidence for a role of Ero1L We analyzed transcriptomic adaptations to hypoxia/reoxygenation in B16 melanoma cells. By Ero1L over- and down-expression in vivo, we identified this ER oxidase as an actor of tumor growth and metastasis take. In vitro culture of B16 submitted to hypoxia (oxygen rate less than 1%)