b16-f10  (ATCC)

Journal: iScience

Article Title: Targeting ADAR1 p150 triggers tumor inhibition and antitumor immunity to overcome immunotherapy resistance

doi: 10.1016/j.isci.2026.115978

Figure Lengend Snippet: p150 depletion is sufficient to inhibit tumor growth inhibition and induce tumor inflammation (A) Schematic of the experimental design using syngeneic transplant models in IFN-β/Luc reporter mice. (B) Tumor growth curves of wild-type versus ADAR1-knockout B16-F10 cells in C57BL/6 mice ( n = 10 mice per group). Data are mean ± SEM. Statistical significance was determined by two-way ANOVA (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (C and D) In vivo bioluminescence imaging (D) and quantification of photon flux (E) from tumors in IFN-β/Luc reporter mice bearing WT or ADAR1-KO B16-F10 tumors ( n = 5 mice per group). Data are mean ± SD. Unpaired t test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (E) Flow cytometric analysis of tumor-infiltrating leukocytes in WT and ADAR1-KO B16-F10 tumors ( n = 4 tumors per group from two independent experiments). (F) Cytokine levels of IFN-β and CXCL10 in tumor homogenates measured by MultiPlex ( n = 5 tumors per group). Data are mean ± SD. Unpaired t test (∗∗ p < 0.01, ∗∗∗ p < 0.001). (G and H) Interferon-stimulated genes (ISGs) expression (H) and heatmap of DEGs with corresponding gene enrichment analysis (I) of RNA-seq data from WT and ADAR1-KO B16-F10 cells ( n = 2 biological replicates per group), showing upregulation of ISGs and dsRNA sensing pathways.

Article Snippet: Mouse: B16-F10 (Melanoma) , ATCC , CRL-6475.

Techniques: Inhibition, Knock-Out, In Vivo, Imaging, Multiplex Assay, Expressing, RNA Sequencing

Journal: iScience

Article Title: Targeting ADAR1 p150 triggers tumor inhibition and antitumor immunity to overcome immunotherapy resistance

doi: 10.1016/j.isci.2026.115978

Figure Lengend Snippet: Genetic disruption of the Zα domain inhibits tumor growth and activates anti-tumor immunity (A) Schematic of the B16-F10 cells engineered to express WT ADAR1 p150 or Zα domain mutants (N175S, Y179A). (B) Heatmap of DEGs between WT and Zα (N175S) mutant cells under basal conditions ( n = 3 biological replicates per group). (C) Gene ontology (GO) enrichment analysis of upregulated pathways in Zα mutant cells compared to WT. (D) Heatmap of ISG upregulation in Zα mutant cells compared to WT under PBS and IFNb condition. (E) Colony formation assay of WT and Zα mutant cells with or without IFN-β treatment. Scale bar, 10 mm. (F) Tumor growth curves of syngeneic mice implanted with B16-F10 cells expressing WT, heterozygous N175S, homozygous Y179A, or homozygous N175S ADAR1 p150 ( n = 8 mice per group). two-way ANOVA ([∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001] for mutants vs. WT). (G) Flow cytometric quantification of tumor-infiltrating leukocytes in WT and Zα (N175S) mutant tumors at endpoint ( n = 6 tumors per group). Data are mean ± SD. two-way ANOVA ([∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001] for mutants vs. WT).

Article Snippet: Mouse: B16-F10 (Melanoma) , ATCC , CRL-6475.

Techniques: Disruption, Mutagenesis, Colony Assay, Expressing

Journal: Molecular Therapy Oncology

Article Title: Oncolytic virotherapy mobilizes tumor-resident, granzyme B-producing bystander CD4 + T cells to inhibit systemic microbial infection

doi: 10.1016/j.omton.2026.201187

Figure Lengend Snippet: Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with B16F10 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.

Article Snippet: B16F10 (CRL-6475) cells were acquired from ATCC.

Techniques: Infection, Isolation, Injection, Control