Abstract: The present invention is directed to association of nuclear receptor tyrosine kinase, such as EGFR, with highly proliferative tissue following its translocation from the cell membrane. The nuclear localization of the receptor tyrosine kinase is affiliated with transcription activity, and the specific sequence associated with such activity, particularly for EGFR, is disclosed.

Abstract: The present invention relates generally to the fields of cancer therapy and gene therapy. More particularly, it demonstrates that PEA3, as exemplified by mPEA3 and hPEA3, is a tumor suppressor and may be used to treat various forms of cancer, for example neu- or ras-mediated cancers.

Abstract: The invention provides E1A gene based anti-cancer therapy that targets cancers and tumors involving phospho-Akt expression (and/or Akt activation) and/or phospho-p38 downregulation (and/or p38 inactivation).

Abstract: The present invention relates to methods for the inhibition, of the gene product of the neu oncogene, p185neu tyrosine kinase. Over-expression of the neu oncogene leads to chemoresistance. The methods disclosed involve the novel use of E1A and/or LT in combination with chemotherapeutic drugs to treat carcinoma. Furthermore, E1A surprisingly potentiates the antineoplastic effects of the chemotherapeutic agents. The inventors propose that E1A sensitizes cancer cells such that they become amenable to treatment by chemotherapeutic drugs.

Abstract: The present invention relates generally to the fields of cancer therapy and gene therapy. More particularly, the invention demonstrates methods for repressing or preventing transformation and proliferation of tumor cells. The method comprises contacting a cell with a p202 polypeptide in an amount effective to inhibit a transformed phenotype or cell proliferation. Inhibition of transformation may be indicated by a reduction in a transforming, tumorigenic or metastatic potential of a cell.

Abstract: The present invention relates generally to the fields of cancer therapy and gene therapy. More particularly, it demonstrates that PEA3, as exemplified by mPEA3 and hPEA3, is a tumor suppressor and may be used to treat various forms of cancer, for example neu- or ras-mediated cancers.

Abstract: The present invention provides methods and compositions for the suppression of oncogenic transformation, tumorigenesis and metastasis. The present invention discloses functional domains of E1A responsible for the suppression of transformation, and provides mini-E1A constructs that can be used for tumor suppression. The invention also discloses methods for the novel use of mini-E1A in combination with chemotherapeutic drugs and/or tyrosine kinase inhibitors.

Abstract: The present invention relates generally to the fields of cancer therapy and gene therapy. More particularly, it demonstrates that PEA3 is a tumor suppressor and may be used to treat various forms of cancer, and especially neu-mediated cancer.

Abstract: The present invention relates generally to the fields of cancer therapy and gene therapy. More particularly, it demonstrates that PEA3 is a tumor suppressor and may be used to treat various forms of cancer, and especially neu-mediated cancer.

Abstract: Disclosed are methods and compositions for the suppression of expression of the neu oncogene, as well as suppression of neu oncogene-mediated transformation, tumorigenesis and metastasis. The method disclosed involves introduction of adenovirus early 1A gene (the E1A gene) products, or the large T antigen (the LT gene product), or both into affected cells. These products, which are preferably introduced by transfection of the E1A gene into affected cells, serve to suppress neu gene expression as measured by a reduction of p185 expression. Furthermore, the E1A gene products surprisingly serve to suppress the oncogenic phenotype, as indicated by a reduction in cell growth, growth in soft agar, as well as tumorigenic and metastatic potential in vivo. The inventors propose that E1A gene products, LT gene products or derivatives therefrom, may ultimately be employed a treatment modalities for neu-mediated cancers, such as cancers of the female genital tract and breast.

Abstract: A tumor necrosis factor (TNF) preparation with high cytolytic activity is described. The TNF preparation includes modified forms of TNF associated with or encapsulated within liposomes. The TNF molecule is modified at up to 3 amino acid residues per trimer with nearly complete retention (80-95%) of biological activity. Amino acid residues of the TNF are modified to include long chain fatty acids via TNF lysyl side chains and/or N-terminal amino acid groups. The disclosed modified TNF molecules provide a highly efficient method for preparing liposome-associated or encapsulated TNF complexes in either standard multilamellar vesicles (MLVs) or small unilamellar vesicles (SUVs) having enhanced in vivo stability. The liposomes of the present invention feature particularly small diameters in the range of 0.02-0.05 um in diameter. The binding of the modified TNF molecules to the surface of SUVs is up to 100% efficiency.

Abstract: Disclosed are methods and compositions for the suppression of expression of the neu oncogene, as well as suppression of neu oncogene-mediated transformation, tumorigenesis and metastasis. The method disclosed involved introduction of adenovirus early 1A gene (the E1A gene) products into affected cells. These products, which are preferably introduced by transfection of the E1A gene into affected cells, serve to suppress neu gene expression as measured by a reduction of p185 expression. Furthermore, the E1A gene products surprisingly serve to suppress the oncogenic phenotype, as indicated by a reduction in cell growth, growth in soft agar, as well as tumorigenic and metastatic potential in vivo. The inventors propose that E1A gene products, or derivatives therefrom, may ultimately be employed a treatment modalities for neu-mediated cancers, such as cancers of the female genital tract and breast.

Abstract: Disclosed are methods and compositions for the suppression of expression of the neu oncogene, as well as suppression of neu oncogene-mediated transformation, tumorigenesis and metastasis. The method disclosed involves introduction of adenovirus early 1A gene (the E1A gene) products, or the large T antigen (the LT gene product), or both into affected cells. These products, which are preferably introduced by transfection of the E1A gene into affected cells, serve to suppress neu gene expression as measured by a reduction of p185 expression. Furthermore, the E1A gene products surprisingly serve to suppress the oncogenic phenotype, as indicated by a reduction in cell growth, growth in soft agar, as well as tumorigenic and metastatic potential in vivo. The inventors propose that E1A gene products, LT gene products or derivatives therefrom, may ultimately be employed a treatment modalities for neu-mediated cancers, such as cancers of the female genital tract and breast.

Abstract: Disclosed are methods and compositions for the suppression of expression of the neu oncogene, as well as suppression of neu oncogene-mediated transformation, tumorigenesis and metastasis. The method disclosed involves introduction of adenovirus early 1A gene (the E1A gene) products, so to large T antigen (the LT gene product), or both into affected cells. These products, which are preferably introduced by transfection of the E1A gene into affected cells, serve to suppress neu gene expression as measured by a reduction of p185 expression. Furthermore, the E1A gene products surprisingly serve to suppress the oncogenic phenotype, as indicated by a reduction in cell growth, growth in soft agar, as well as tumorigenic and metastatic potential in vivo. The inventors propose that E1A gene products, LT gene products or derivatives therefrom, may ultimately be employed a treatment modalities for neu-mediated cancers, such as cancers of the female genital tract and breast.