Patents by Inventor Tapas Mukhopadhyay
Tapas Mukhopadhyay 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).
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Patent number: 7423015Abstract: The present invention is directed to the use of benzimidazole derivatives for the treatment of tumors and in combination with tumor suppressor gene therapy. In a particular embodiment, treatment of p53-positive tumors with benzimidazole derivatives induces p53 expression and increases its half-life, resulting in apoptotic death of the tumor cells. Similarly, in conjunction with p53 gene therapy, benzimidazole derivatives induce p53 expression and accumulation in tumor cells regardless of their p53 status. The combination treatment subsequently elicits apoptosis of the tumor cells.Type: GrantFiled: January 9, 2002Date of Patent: September 9, 2008Assignees: Board of Regents, The University of Texas System, Introgen Therapeutics, Inc.Inventors: Tapas Mukhopadhyay, Sunil Chada, Abner Mhashilkar, Jack A. Roth
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Patent number: 7109179Abstract: The present invention relates to the use of tumor suppressor genes in combination with a DNA damaging agent or factor for use in killing cells, and in particular cancerous cells. A tumor suppressor gene, p53, was delivered via a recombinant adenovirus-mediated gene transfer both in vitro and in vivo, in combination with a chemotherapeutic agent. Treated cells underwent apoptosis with specific DNA fragmentation. Direct injection of the p53-adenovirus construct into tumors subcutaneously, followed by intraperitoneal administration of a DNA damaging agent, cisplatin, induced massive apoptotic destruction of the tumors. The invention also provides for the clinical application of a regimen combining gene replacement using replication-deficient wild-type p53 adenovirus and DNA-damaging drugs for treatment of human cancer.Type: GrantFiled: February 23, 2004Date of Patent: September 19, 2006Assignee: Board of Regents, the University of Texas SystemInventors: Jack A. Roth, Toshiyoshi Fujiwara, Elizabeth A. Grimm, Tapas Mukhopadhyay, Wei-Wei Zhang, Laurie B. Owen-Schaub
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Publication number: 20060182718Abstract: The present invention relates to the use of tumor suppressor genes in combination with a DNA damaging agent or factor for use in killing cells, and in particular cancerous cells. A tumor suppressor gene, p53, was delivered via a recombinant adenovirus-mediated gene transfer both in vitro and in vivo, in combination with a chemotherapeutic agent. Treated cells underwent apoptosis with specific DNA fragmentation. Direct injection of the p53-adenovirus construct into tumors subcutaneously, followed by intraperitoneal administration of a DNA damaging agent, cisplatin, induced massive apoptotic destruction of the tumors. The invention also provides for the clinical application of a regimen combining gene replacement using replication-deficient wild-type p53 adenovirus and DNA-damaging drugs for treatment of human cancer.Type: ApplicationFiled: February 6, 2006Publication date: August 17, 2006Inventors: Jack Roth, Toshiyoshi Fujiwara, Elizabeth Grimm, Tapas Mukhopadhyay, Wei-Wei Zhang, Laurie Owen-Schaub
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Patent number: 6998117Abstract: Disclosed are methods and compositions for the selective manipulation of gene expression through the preparation of retroviral expression vectors for expressing antisense sequences, such as K-ras oncogene antisense sequences, or sequences encoding a desired product, such as wild type p53 sequences. Preferred retroviral vectors of the present invention incorporate the ?-actin promoter in a reverse orientation with respect to retroviral transcription. Preferred antisense RNA constructs of the present invention employ the use of antisense intron DNA corresponding to distinct intron regions of the gene whose expression is targeted for down-regulation. In an exemplary embodiment, a human lung cancer cell line (NCI-H460a) with a homozygous spontaneous K-ras mutation was transfected with a recombinant plasmid that synthesizes a genomic segment of K-ras in antisense orientation. Translation of the mutated K-ras mRNA was specifically inhibited, whereas expression of H-ras and N-ras was unchanged.Type: GrantFiled: June 2, 1995Date of Patent: February 14, 2006Assignee: Board of Regents, The University of Texas SystemInventors: Jack A. Roth, Tapas Mukhopadhyay, Michael A. Tainsky
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Publication number: 20050089511Abstract: The present invention relates to the use of tumor suppressor genes in combination with a DNA damaging agent or factor for use in killing cells, and in particular cancerous cells. A tumor suppressor gene, p53, was delivered via a recombinant adenovirus-mediated gene transfer both in vitro and in vivo, in combination with a chemotherapeutic agent. Treated cells underwent apoptosis with specific DNA fragmentation. Direct injection of the p53-adenovirus construct into tumors subcutaneously, followed by intraperitoneal administration of a DNA damaging agent, cisplatin, induced massive apoptotic destruction of the tumors. The invention also provides for the clinical application of a regimen combining gene replacement using replication-deficient wild-type p53 adenovirus and DNA-damaging drugs for treatment of human cancer.Type: ApplicationFiled: February 23, 2004Publication date: April 28, 2005Inventors: Jack Roth, Toshiyoshi Fujiwara, Elizabeth Grimm, Tapas Mukhopadhyay, Wei-Wei Zhang, Laurie Owen-Schaub
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Patent number: 6797702Abstract: The present invention relates to the use of tumor suppressor genes in combination with a DNA damaging agent or factor for use in killing cells, and in particular cancerous cells. A tumor suppressor gene, p53, was delivered via a recombinant adenovirus-mediated gene transfer both in vitro and in vivo, in combination with a chemotherapeutic agent. Treated cells underwent apoptosis with specific DNA fragmentation. Direct injection of the p53-adenovirus construct into tumors subcutaneously, followed by intraperitoneal administration of a DNA damaging agent, cisplatin, induced massive apoptotic destruction of the tumors. The invention also provides for the clinical application of a regimen combining gene replacement using replication-deficient wild-type p53 adenovirus and DNA-damaging drugs for treatment of human cancer.Type: GrantFiled: August 26, 1997Date of Patent: September 28, 2004Assignee: Board of Regents, The University of Texas SystemInventors: Jack A. Roth, Toshiyoshi Fujiwara, Elizabeth A. Grimm, Tapas Mukhopadhyay, Wei-Wei Zhang, Laurie B. Owen-Schaub
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Publication number: 20030099614Abstract: The present invention details methods for the treatment of cancer. In particular, it concerns the induction of apoptosis of cancer cells following treatment with methoxyestradiol. 2-methoxyestradiol (2-MeOE2) increase wild-type p53 levels in a human non-small lung cancer cell lines associated with accumulation of cyclin dependent kinase inhibitor p21WAF1/CIP1. Significant apoptotic cell death occurred after the drug treatment. Thus, 2-MeOE2 facilitates induction of p53-mediated apoptosis.Type: ApplicationFiled: June 25, 2002Publication date: May 29, 2003Applicant: Board of Regents, The University of Texas SystemInventors: Tapas Mukhopadhyay, Jack A. Roth
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Patent number: 6482803Abstract: The present invention discloses expression constructs and methods for employing them that result in the modulation of abnormal oncogene and tumor suppressor genes in a novel approach to cancer prevention and therapy. In one embodiment, an expression construct expresses a ribozyme that inactivates mutant p53 and also expresses the functional p53.Type: GrantFiled: September 1, 1995Date of Patent: November 19, 2002Assignee: Board of Regents, The University of Texas SystemInventors: Jack A. Roth, De Wei Cai, Tapas Mukhopadhyay
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Patent number: 6410029Abstract: The present invention details methods for the treatment of cancer. In particular, it concerns the induction of apoptosis of cancer cells following treatment with methoxyestradiol. 2-methoxyestradiol (2-MeOE2) increase wild-type p53 levels in a human non-small lung cancer cell lines associated with accumulation of cyclin dependent kinase inhibitor p21 WAF1/CIP1. Significant apoptotic cell death occurred after the drug treatment. Thus, 2-MeOE2 facilitates induction of p53-mediated apoptosis.Type: GrantFiled: July 9, 1999Date of Patent: June 25, 2002Assignee: Board of Regents, The University of Texas SystemInventors: Tapas Mukhopadhyay, Jack A. Roth
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Patent number: 6069134Abstract: The present invention relates to the use of tumor suppressor genes in combination with a DNA damaging agent or factor for use in killing cells, and in particular cancerous cells. A tumor suppressor gene, p53, was delivered via a recombinant adenovirus-mediated gene transfer both in vitro and in vivo, in combination with a chemotherapeutic agent. Treated cells underwent apoptosis with specific DNA fragmentation. Direct injection of the p53-adenovirus construct into tumors subcutaneously, followed by intraperitoneal administration of a DNA damaging agent, cisplatin, induced massive apoptotic destruction of the tumors. The invention also provides for the clinical application of a regimen combining gene replacement using replication-deficient wild-type p53 adenovirus and DNA-damaging drugs for treatment of human cancer.Type: GrantFiled: October 17, 1997Date of Patent: May 30, 2000Assignee: Board of Regents, The University of Texas SystemInventors: Jack A. Roth, Toshiyoshi Fujiwara, Elizabeth A. Grimm, Tapas Mukhopadhyay, Wei-Wei Zhang, Laurie B. Owen-Schaub
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Patent number: 6017524Abstract: Disclosed are methods and compositions for the selective manipulation of gene expression through the preparation of retroviral expression vectors for expressing antisense sequences, such as K-ras oncogene antisense sequences, or sequences encoding a desired product, such as wild type p53 sequences. Preferred retroviral vectors of the present invention incorporate the .beta.-actin promoter in a reverse orientation with respect to retroviral transcription. Preferred antisense RNA constructs of the present invention employ the use of antisense intron DNA corresponding to distinct intron regions of the gene whose expression is targeted for down-regulation. In an exemplary embodiment, a human lung cancer cell line (NCI-H460a) with a homozygous spontaneous K-ras mutation was transfected with a recombinant plasmid that synthesizes a genomic segment of K-ras in antisense orientation. Translation of the mutated K-ras mRNA was specifically inhibited, whereas expression of H-ras and N-ras was unchanged.Type: GrantFiled: October 13, 1992Date of Patent: January 25, 2000Assignee: Board of Regents, The University of Texas SystemInventors: Jack A. Roth, Tapas Mukhopadhyay, Michael A. Tainsky
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Patent number: 5958892Abstract: The present invention details methods for the treatment of cancer. In particular, it concerns the induction of apoptosis of cancer cells following treatment with methoxyestradiol. 2-methoxyestradiol (2-MeOE.sub.2) increase wild-type p53 levels in a human non-small lung cancer cell lines associated with accumulation of cyclin dependent kinase inhibitor p21 WAF1/CIP1. Significant apoptotic cell death occurred after the drug treatment. Thus, 2-MeOE.sub.2 facilitates induction of p53-mediated apoptosis.Type: GrantFiled: July 30, 1996Date of Patent: September 28, 1999Assignee: Board of Regents, The University of Texas SystemInventors: Tapas Mukhopadhyay, Jack A. Roth
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Patent number: 5747469Abstract: The present invention relates to the use of tumor suppressor genes in combination with a DNA damaging agent or factor for use in killing cells, and in particular cancerous cells. A tumor suppressor gene, p53, was delivered via a recombinant adenovirus-mediated gene transfer both in vitro and in vivo, in combination with a chemotherapeutic agent. Treated cells underwent apoptosis with specific DNA fragmentation. Direct injection of the p53-adenovirus construct into tumors subcutaneously, followed by intraperitoneal administration of a DNA damaging agent, cisplatin, induced massive apoptotic destruction of the tumors. The invention also provides for the clinical application of a regimen combining gene replacement using replication-deficient wild-type p53 adenovirus and DNA-damaging drugs for treatment of human cancer.Type: GrantFiled: April 25, 1994Date of Patent: May 5, 1998Assignee: Board of Regents, The University of Texas SystemInventors: Jack A. Roth, Toshiyoshi Fujiwara, Elizabeth A. Grimm, Tapas Mukhopadhyay, Wei-Wei Zhang, Laurie B. Owen-Schaub