Abstract: Provided herein are compositions and methods for the treatment of cancer by inhibition of ?-catenin or a ?-catenin pathway. In particular, inhibitors of ?-catenin and/or the Wnt/?-catenin signaling pathway are employed prevent or reverse evasion of immune response or immunotherapy by cancers.

Abstract: Provided herein are compositions and methods for detecting and/or targeting dysfunctional tumor antigen-specific CD8+ T cells in the tumor microenvironment for diagnostic, therapeutic and/or research applications. In particular, dysfunctional tumor antigen-specific CD8+ T cells are detected and/or targeted via their expression of cell surface receptors described herein, such as 4-1BB, LAG-3, or additional markers that correlate with 4-1BB and LAG-3 expression, such as markers differentially expressed on the surface of the T cells.

Abstract: Provided herein are compositions and methods for detecting and/or targeting dysfunctional tumor antigen-specific CD8+ T cells in the tumor microenvironment for diagnostic, therapeutic and/or research applications. In particular, dysfunctional tumor antigen-specific CD8+ T cells are detected and/or targeted via their expression of cell surface receptors described herein, such as 4-1BB, LAG-3, or additional markers that correlate with 4-1BB and LAG-3 expression, such as markers differentially expressed on the surface of the T cells.

Abstract: Provided herein are compositions and methods for the treatment of cancer by inhibition of ?-catenin or a ?-catenin pathway. In particular, inhibitors of ?-catenin and/or the Wnt/?-catenin signaling pathway are employed prevent or reverse evasion of immune response or immunotherapy by cancers.

Abstract: Provided herein are compositions and methods for the treatment of cancer by inhibition of ?-catenin or a ?-catenin pathway. In particular, inhibitors of ?-catenin and/or the Wnt/p-catenin signaling pathway are employed prevent or reverse evasion of immune response or immunotherapy by cancers.

Abstract: Provided herein are compositions and methods for detecting and/or targeting dysfunctional tumor antigen-specific CD8+ T cells in the tumor microenvironment for diagnostic, therapeutic and/or research applications. In particular, dysfunctional tumor antigen-specific CD8+ T cells are detected and/or targeted via their expression of cell surface receptors described herein, such as 4-1BB, LAG-3, or additional markers that correlate with 4-1BB and LAG-3 expression, such as markers differentially expressed on the surface of the T cells.

Abstract: Provided herein are compositions and methods for the treatment of cancer by inhibition of ?-catenin or a ?-catenin pathway. In particular, inhibitors of ?-catenin and/or the Wnt/p-catenin signaling pathway are employed prevent or reverse evasion of immune response or immuno-therapy by cancers.

Abstract: A catalytic reactor having a mixing section connected to a downstream reaction section containing a catalyst to promote a reaction of oxygen and a hydrocarbon fed to the catalytic reactor. The mixing section is provided with a flame arrestor to prevent a stable flame from propagating should any reaction of oxygen and hydrocarbons occur during mixing. The flame arrestor permits flow in both axial and radial directions to promote mixing. Baffle elements and a downstream static mixer can also be used. The catalyst is preferably in the form of monolithic blocks enclosed by a ceramic tube that is maintained as a unitary catalyst assembly that can be removed for replacement and installation of the catalyst as a single unit.

Abstract: T cell anergy has been correlated with defective Ras signaling. However, neither a causal relationship nor the mechanism of Ras hypoactivation have been established. Using adenoviral transduction of CAR Tg T cells to enable genetic manipulation in nonproliferating cells, we show that Ras61L restores IL-2 production and MAP kinase signaling in T cells anergized in vitro or in vivo. A gene array screen revealed upregulated diacylglycerol kinase (DGK) in the anergic state, which was confirmed by RT-PCR and Western blot analysis. A DGK inhibitor significantly restored IL-2 production by anergic cells. Our data support a causal role for DGK and defective Ras signaling in T cell anergy.

Abstract: The present invention provides novel panels of molecular targets that are differentially expressed during CD8+ T cell priming. The novel panels of the invention may be used, for example, in therapeutic intervention, therapeutic agent screening, and in diagnostic methods for diseases and/or disorders of the immune system.

Abstract: Complexes of SEQ ID NO: 12 and HLA-A2 can be used to generate CTLs. They can be supplemented with IL-6 and IL-12.

Abstract: Tumor rejection antigens derived from MAGE tumor rejection precursors have been identified. These "TRAS" bind to the MHC-class I molecule HLA-A2, and the resulting complexes stimulate the production of cytolytic T cell clones which lyse the presenting cells. The peptides and complexes may be used diagnostically, therapeutically, and as immunogens for the production of antibodies, or as targets for the generation of cytolytic T cell clones.

Abstract: Tumor rejection antigens derived from tumor rejection precursor MAGE-3 have been identified. These "TRAS" bind to the MHC-class I molecule HLA-A2, and the resulting complexes stimulate the production of cytolytic T cell clones which lyse the presenting cells. The peptides and complexes may be used diagnostically, therapeutically, and as immunogens for the production of antibodies, or as targets for the generation of cytolytic T cell clones.