Abstract: Microbubble-assisted delivery of viruses is disclosed. In particular, methods for targeting a virus to cancer cells in an immunocompetent animal by administering a selectively replicating virus to the immunocompetent animal and disrupting the microbubbles in a location of the animal comprising cancer cells are provided. The virus is encompassed in a suspension of microbubbles, and the surface of the suspension does not include any virus. A suspension of microbubbles comprising a selectively replicating virus that is encompassed in a suspension of microbubbles, which does not include any virus on the surface of the suspension, is also provided.

Abstract: Methods, compositions, and therapeutic products for use in the field of oncology and specifically, for the treatment of cancer and other diseases in which SARI is ameliorative or therapeutic and/or small molecule screening for anti-cancer drugs are provided. Cancer specific gene expression using the CCN1 promoter, which is negatively regulated by SARI, for targeting therapeutic molecules in tumors is also provided.

Abstract: The present invention relates to viral vectors that are targeted to cancer cells. The viral vectors of the invention are adenoviruses having a PEG-3 promoter driving the expression of the viral genes E1A and E1B. The PEG-3 promoter exhibits increased activity in malignant cells. Adenoviruses of the invention show increased replication in malignant cells, thereby producing a cytopathic effect. The viral vectors of the invention further comprise additional genes of interest, and/or may have altered capsid proteins that may enhance infection of and/or target infection to cancer cells. Additional cell types derived from diseased states in which the PEG-3 promoter is selectively active are also therapeutic targets of the viral vectors of the instant invention including those generating allergic, autoimmune and inflammatory responses.

Abstract: The present invention relates to the discovery that OLD-35, at least in part through the generation of reactive oxygen species, induces a number of inflammatory cytokines and promotes nuclear translocation and binding of the transcriptional activator NF-?B. Accordingly, the present invention provides for assay systems (which either utilize the old-35 promoter or the old-35 gene) that may be used to identify new anti-inflammatory agents; model systems of inflammation based on over-expression of the old-35 gene in cells and tissues (including specific model systems for arthritis, atherosclerosis and Alzheimer's disease); methods and kits for diagnosing old-35 associated inflammatory conditions, and methods of treatment and anti-inflammatory compositions that utilize agents that antagonize OLD-35 activity.

Abstract: The present invention relates to the old-35 gene, its encoded protein, and its promoter sequence.

Abstract: The present invention relates to viral vectors that are targeted to cancer cells. The viral vectors of the invention are adenoviruses having a PEG-3 promoter driving the expression of the viral genes E1A and E1B. The PEG-3 promoter exhibits increased activity in malignant cells. Adenoviruses of the invention show increased replication in malignant cells, thereby producing a cytopathic effect. The viral vectors of the invention may comprise additional genes of interest, and/or may have altered capsid proteins that may enhance infection of and/or target infection to cancer cells. Additional cell types derived from diseased states in which the PEG-3 promoter is selectively active are also therapeutic targets of the viral vectors of the instant invention including those generating allergic, autoimmune and inflammatory responses.

Abstract: The present invention relates to the discoveries that apoptotic effects of the melanoma differentiation associated gene mda-7 (also known as interleukin-24, “IL-24”) on malignant cells occur via the p38 MAPK pathway and members of the Growth Arrest and DNA Damage (“GADD”) gene family but are substantially independent of the JAK/STAT pathway. Accordingly, the invention provides for methods for identifying apoptosis-modulating agents using assay methods which determine the ability of a test agent to increase or decrease expression of constituents of the mda-7 apoptosis pathway, preferably in a JAK/STAT substantially independent manner. Such agents may be small molecules or may be fragments, variants and/or derivatives of native MDA-7.