MD Anderson Cancer Center 1515 Holcombe Blvd Suite 207, Houston, TX 77030 (713)7922121 (Phone)
Conditions:
Congestive Heart Failure
Certifications:
General Surgery, 1981 Thoracic Cardiovascular Surgery, 1983
Awards:
Healthgrades Honor Roll
Languages:
English
Hospitals:
Houston Office 1515 Holcombe Blvd Suite 10, Houston, TX 77030
MD Anderson Cancer Center 1515 Holcombe Blvd Suite 207, Houston, TX 77030
Montefiore Medical Center 111 East 210Th Street, Bronx, NY 10467
Saint Joseph's Medical Center 127 South Broadway, Yonkers, NY 10701
Education:
Medical School Johns Hopkins University / School of Medicine Graduated: 1971 Medical School The Johns Hopkins Hospital Graduated: 1971 Medical School UCLA Ctr Hlth Scis Graduated: 1971 Medical School UCLA Div Surg Onc Graduated: 1971
Jack Roth, Houston TX
Work:
MD Anderson Cancer Ctr
1515 Holcombe Blvd, Houston, TX 77030
Name / Title
Company / Classification
Phones & Addresses
Jack Roth
Innovation Plus Developments Ltd Contractors - General
Wei-Wei Zhang - Sugar Land TX Jack A Roth - Houston TX
Assignee:
Board of Regents, The University of Texas System - Austin TX
International Classification:
A61K 4800
US Classification:
424 932, 424 931, 424 936, 4353201
Abstract:
Described are simplified and efficient methods for preparing recombinant adenovirus using liposome-mediated cotransfection and the direct observation of a cytopathic effect (CPE) in the transfected cells. Also disclosed are compositions and methods involving novel p53 adenovirus constructs, including methods for restoring p53 function and tumor suppression in cells and animals having abnormal p53.
2-Methoxyestradiol-Induced Apoptosis In Cancer Cells
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 ) 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 facilitates induction of p53-mediated apoptosis.
Jack A. Roth - Houston TX Tapas Mukopadhyay - Houston TX Michael Tainsky - Houston TX
Assignee:
Board of Regents, The University of Texas Systems - Austin TX
International Classification:
C12N 1500
US Classification:
4353201, 536 245
Abstract:
Disclosed are methods and compositions for the selective inhibition gene expression through the application of antisense RNA technology. 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. A three-fold growth inhibition occurred in H460a cells when expression of the mutated ras p21 protein was down-regulated by antisense RNA and cells remained viable. The growth of H460a tumors in nu/nu mice was substantially reduced by expressed K-ras antisense RNA.
Modification Of Mutated P53 Gene In Tumors By Retroviral Delivery Of Ribozyme A
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.
Recombinant P53 Adenovirus Methods And Compositions
Described are simplified and efficient methods for preparing recombinant adenovirus using liposome-mediated cotransfection and the direct observation of a cytopathic effect (CPE) in the transfected cells. Also disclosed are compositions and methods involving novel p53 adenovirus constructs, including methods for restoring p53 function and tumor suppression in cells and animals having abnormal p53.
Inhibition Of Cellular Proliferation Using Ras Antisense Molecules
Jack A. Roth - Houston TX Tapas Mukopadhyay - Houston TX Michael Tainsky - Houston TX
Assignee:
Board of Regents, The University of Texas Systems - Austin TX
International Classification:
A01N 6300
US Classification:
424 932, 514 44
Abstract:
Disclosed are methods and compositions for the selective inhibition gene expression through the application of antisense RNA technology. 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. A three-fold growth inhibition occurred in H460a cells when expression of the mutated ras p21 protein was down-regulated by antisense RNA and cells remained viable. The growth of H460a tumors in nu/nu mice was substantially reduced by expressed K-ras antisense RNA.
Diminishing Viral Gene Expression By Promoter Replacement
Bingliang Fang - Houston TX Jack A. Roth - Houston TX
Assignee:
Texas Systems, University of the Board of Regents - Austin TX
International Classification:
C12N 15861
US Classification:
4353201, 536 235, 536 2372, 536 241
Abstract:
The present invention provides viral vectors that have been engineered to contain a synthetic promoter that controls at least one essential gene. The synthetic promoter is induced by a specific gene product not normally produced in the cells in which the viral vector is to be transferred. The vectors are propagated in producer or helper cells that express the inducing factor, thereby permitting the virus to replicate to high titer. The lack of the inducing factor in the target cells precludes viral replication, however, meaning that no vector toxicity or immunogenicity arises. Where the virus carries a gene of interest, this should provide for higher level expression for longer periods of time than with current vectors. Methods for making the vectors, helper cells, and their use in protein production, vaccines and gene therapy are disclosed.
Recombinant P53 Adenovirus Methods And Compositions
Described are simplified and efficient methods for preparing recombinant adenovirus using liposome-mediated cotransfection and the direct observation of a cytopathic effect (CPE) in the transfected cells. Also disclosed are compositions and methods involving novel p53 adenovirus constructs, including methods for restoring p53 function and tumor suppression in cells and animals having abnormal p53.
Sir George Williams High School Montreal Kuwait 1946-1950
Community:
John Foster, Eigil Pedersen, Florence Shaw, Margaret Dufays, Gordon Rabey, Alan Mckeown, Nancy Miller, Edwin Isaacson, Rolande Kursner, Carol Dudley, Elizabeth Noll