Florian Kühnel
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View article: A preclinical model for the identification of therapeutically active transgenes in local cancer immunotherapy
A preclinical model for the identification of therapeutically active transgenes in local cancer immunotherapy Open
The efficacy of systemic immunotherapies is limited for poorly immunogenic tumors which suppress T cell priming and tumor infiltration. Modern antigen carriers including viral vectors and messenger RNA/lipid nanoparticle (LNP) combinations…
View article: Enhancement of colorectal cancer therapy through interruption of the HSF1-HSP90 axis by p53 activation or cell cycle inhibition
Enhancement of colorectal cancer therapy through interruption of the HSF1-HSP90 axis by p53 activation or cell cycle inhibition Open
The stress-associated chaperone system is an actionable target in cancer therapies. It is ubiquitously upregulated in cancer tissues and enables tumorigenicity by stabilizing oncoproteins. Most inhibitors target the key component, heat-sho…
View article: Oncolytic viruses expressing MATEs facilitate target-independent T-cell activation in tumors
Oncolytic viruses expressing MATEs facilitate target-independent T-cell activation in tumors Open
Oncolytic viruses (OV) expressing bispecific T-cell engagers (BiTEs) are promising tools for tumor immunotherapy but the range of target tumors is limited. To facilitate effective T-cell stimulation with broad-range applicability, we estab…
View article: Sequential STING and CD40 agonism drives massive expansion of tumor-specific T cells in liposomal peptide vaccines
Sequential STING and CD40 agonism drives massive expansion of tumor-specific T cells in liposomal peptide vaccines Open
The clinical use of cancer vaccines is hampered by the low magnitude of induced T-cell responses and the need for repetitive antigen stimulation. Here, we demonstrate that liposomal formulations with incorporated STING agonists are optimal…
View article: Phosphatidylinositol 4-Kinase III Alpha Governs Cytoskeletal Organization for Invasiveness of Liver Cancer Cells
Phosphatidylinositol 4-Kinase III Alpha Governs Cytoskeletal Organization for Invasiveness of Liver Cancer Cells Open
View article: Enhancement of colorectal cancer therapy through interruption of the HSF1-HSP90 axis by p53 activation or cell cycle inhibition
Enhancement of colorectal cancer therapy through interruption of the HSF1-HSP90 axis by p53 activation or cell cycle inhibition Open
The stress-associated molecular chaperone system is an actionable target in cancer therapies. It is ubiquitously upregulated in cancer tissues and enables tumorigenicity by stabilizing hundreds of oncoproteins and disturbing the stoichiome…
View article: Interfering with ß-catenin-induced immunosuppression in HCC by cytokine-armed virotherapy
Interfering with ß-catenin-induced immunosuppression in HCC by cytokine-armed virotherapy Open
Mutations of β-catenin are frequent in HCC and are involved in dysfunctional antigen presentation, immunosuppression, and insensitivity to immunotherapies. Animal models of HCC with defined immunogenicity and dysfunctional Wnt/β-catenin ac…
View article: Phosphatidylinositol 4-kinase III alpha governs cytoskeletal organization for invasiveness of liver cancer cells
Phosphatidylinositol 4-kinase III alpha governs cytoskeletal organization for invasiveness of liver cancer cells Open
Background and Aims High expression of phosphatidylinositol 4-kinase III alpha (PI4KIIIα) correlates with poor survival rates in patients with hepatocellular carcinoma (HCC). In addition, Hepatitis C virus (HCV) infections activate PI4KIII…
View article: Supplementary Figure S5 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S5 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S5. Anti-CD96 combines with anti-CTLA4 or anti-PD1 to enhance survival following challenge with experimental lung metastases.
View article: Supplementary Figure S2 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S2 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S2. Anti-metastatic activity of anti-CD96 is dependent on NK cells and IL-12p35, but independent of T cells.
View article: Supplementary Figure S2 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S2 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S2. Anti-metastatic activity of anti-CD96 is dependent on NK cells and IL-12p35, but independent of T cells.
View article: Data from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Data from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
CD96 has recently been shown as a negative regulator of mouse natural killer (NK)–cell activity, with Cd96−/− mice displaying hyperresponsive NK cells upon immune challenge. In this study, we have demonstrated that blocki…
View article: Supplementary Figure S6 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S6 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S6. Anti-CD96 combines with anti-CTLA4, anti-PD1 or doxorubicin to increase survival and reduce metastases in mice bearing 4T1.2 spontaneous metastases.
View article: Supplementary Figure S3 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S3 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S3. Cd96-/- mice are resistant to EO771 spontaneous lung metastases and treatment with anti-CD96 mAb does not increase anti-metastatic effect.
View article: Supplementary Figure S3 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S3 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S3. Cd96-/- mice are resistant to EO771 spontaneous lung metastases and treatment with anti-CD96 mAb does not increase anti-metastatic effect.
View article: Supplementary Methods, Figure Legends from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Methods, Figure Legends from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Methods, Figure Legends
View article: Supplementary Figure S4 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S4 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S4. The effect of anti-CD96 combined with anti-PD1 or anti-CTLA4 in reducing experimental lung metastases is additive.
View article: Supplementary Figure S7 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S7 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S7. Reduction in B16F10 lung metastases by anti-CD96/anti-PD1 is dependent on NK cells.
View article: Supplementary Figure S8 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S8 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S8. Anti-CD96 and anti-PD1 therapy does not induce significant toxicities in B16F10 tumor bearing mice.
View article: Supplementary Figure S1 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S1 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S1. CD96 and CD226 have opposite roles in the control of experimental lung tumor metastases.
View article: Supplementary Figure S4 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S4 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S4. The effect of anti-CD96 combined with anti-PD1 or anti-CTLA4 in reducing experimental lung metastases is additive.
View article: Data from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Data from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
CD96 has recently been shown as a negative regulator of mouse natural killer (NK)–cell activity, with Cd96−/− mice displaying hyperresponsive NK cells upon immune challenge. In this study, we have demonstrated that blocki…
View article: Supplementary Methods, Figure Legends from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Methods, Figure Legends from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Methods, Figure Legends
View article: Supplementary Figure S5 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S5 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S5. Anti-CD96 combines with anti-CTLA4 or anti-PD1 to enhance survival following challenge with experimental lung metastases.
View article: Supplementary Figure S8 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S8 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S8. Anti-CD96 and anti-PD1 therapy does not induce significant toxicities in B16F10 tumor bearing mice.
View article: Supplementary Figure S1 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S1 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S1. CD96 and CD226 have opposite roles in the control of experimental lung tumor metastases.
View article: Supplementary Figure S6 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S6 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S6. Anti-CD96 combines with anti-CTLA4, anti-PD1 or doxorubicin to increase survival and reduce metastases in mice bearing 4T1.2 spontaneous metastases.
View article: Supplementary Figure S7 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy
Supplementary Figure S7 from Suppression of Metastases Using a New Lymphocyte Checkpoint Target for Cancer Immunotherapy Open
Supplementary Figure S7. Reduction in B16F10 lung metastases by anti-CD96/anti-PD1 is dependent on NK cells.
View article: Supplementary Figure S5 from Perioperative, Spatiotemporally Coordinated Activation of T and NK Cells Prevents Recurrence of Pancreatic Cancer
Supplementary Figure S5 from Perioperative, Spatiotemporally Coordinated Activation of T and NK Cells Prevents Recurrence of Pancreatic Cancer Open
NK cell cytotoxicity assay
View article: Supplemetary Figure S3 from Perioperative, Spatiotemporally Coordinated Activation of T and NK Cells Prevents Recurrence of Pancreatic Cancer
Supplemetary Figure S3 from Perioperative, Spatiotemporally Coordinated Activation of T and NK Cells Prevents Recurrence of Pancreatic Cancer Open
Immunohistochemical analysis of E-Cadherin expression