Patents by Inventor Robert J. DeFatta

Robert J. DeFatta has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).

  • Patent number: 7592320
    Abstract: A novel gene therapy for cancer has been discovered, which unlike most prior approaches, does not require specific knowledge of the cancer cells, but instead targets a general characteristic that distinguishes cancer cells from normal cells, i.e., elevated eIF4E expression. The expression of a toxin or conditional toxin such as HTK is translationally repressed in normal cells by placing a complex 5? UTR in front of its reading frame. In prototype experiments, this HTK mRNA, a transcriptional product of the BK-UTK vector, was translationally regulated so as to largely inhibit its production in normal murine and human cells, while cancer cells efficiently translated the protein, which a resulting increased sensitivity to GCV. Synthesis of the HTK protein from the BK-UTK vector (containing the 5? UTR of Fibroblast growth factor-2 (“FGF-2”) readily occurred in a panel of murine and human breast carcinoma lines, but not in normal cell lines.
    Type: Grant
    Filed: November 20, 2003
    Date of Patent: September 22, 2009
    Inventors: Arrigo DeBenedetti, Robert J. DeFatta
  • Patent number: 6759394
    Abstract: A novel gene therapy for cancer has been discovered, which unlike most prior appraches, does not require specific knowledge of the cancer cells, but instead targets a general characteristic that distinguishes cancer cells from normal cells, i.e., elevated eIF4E expression. The expression of a toxin or conditional toxin such as HTK is translationally repressed in normal cells by placing a complex 5′ UTR in front of its reading frame. In prototype experiments, this HTK mRNA, a transcriptional product of the BK-UTK vector, was translationally regulated so as to largely inhibit its production in normal murine and human cells, while cancer cells efficiently translated the protein, which a resulting increased sensitivity to GCV. Synthesis of the HTK protein from the BK-UTK vector (containing the 5′ UTR of Fibroblast growth factor −2 (“FGF-2”) readily occurred in a panel of murine and human breast carcinoma lines, but not in normal cell lines.
    Type: Grant
    Filed: July 26, 2001
    Date of Patent: July 6, 2004
    Assignee: Board of Supervisors of La. State Un. & Agricultural and Mechanical College
    Inventors: Arrigo DeBenedetti, Robert J. DeFatta
  • Publication number: 20040110716
    Abstract: A novel gene therapy for cancer has been discovered, which unlike most prior approaches, does not require specific knowledge of the cancer cells, but instead targets a general characteristic that distinguishes cancer cells from normal cells, i.e., elevated eIF4E expression. The expression of a toxin or conditional toxin such as HTK is translationally repressed in normal cells by placing a complex 5′ UTR in front of its reading frame. In prototype experiments, this HTK mRNA, a transcriptional product of the BK-UTK vector, was translationally regulated so as to largely inhibit its production in normal murine and human cells, while cancer cells efficiently translated the protein, which a resulting increased sensitivity to GCV. Synthesis of the HTK protein from the BK-UTK vector (containing the 5′ UTR of Fibroblast growth factor-2 (“FGF-2”) readily occurred in a panel of murine and human breast carcinoma lines, but not in normal cell lines.
    Type: Application
    Filed: November 20, 2003
    Publication date: June 10, 2004
    Inventors: Arrigo DeBenedetti, Robert J. DeFatta
  • Publication number: 20030087852
    Abstract: A novel gene therapy for cancer has been discovered, which unlike most prior appraches, does not require specific knowledge of the cancer cells, but instead targets a general characteristic that distinguishes cancer cells from normal cells, i.e., elevated eIF4E expression. The expression of a toxin or conditional toxin such as HTK is translationally repressed in normal cells by placing a complex 5′ UTR in front of its reading frame. In prototype experiments, this HTK mRNA, a transcriptional product of the BK-UTK vector, was translationally regulated so as to largely inhibit its production in normal murine and human cells, while cancer cells efficiently translated the protein, which a resulting increased sensitivity to GCV. Synthesis of the HTK protein from the BK-UTK vector (containing the 5′ UTR of Fibroblast growth factor −2 (“FGF-2”) readily occurred in a panel of murine and human breast carcinoma lines, but not in normal cell lines.
    Type: Application
    Filed: July 26, 2001
    Publication date: May 8, 2003
    Inventors: Arrigo DeBenedetti, Robert J. DeFatta