Delivery of herpes simplex thymidine kinase bystander effect by engineered human mesothelial cells for the treatment of ovarian cancer

Delivery of herpes simplex thymidine kinase bystander effect by engineered human mesothelial cells for the treatment of ovarian cancer

Delivery of herpes simplex thymidine kinase bystander effect by engineered human mesothelial cells for the treatment of ovarian cancer
COLUMBUS, Ohio – In six out of 10 cases, ovarian cancer is diagnosed when the disease is advanced and five-year survival is only 27 percent. Both wild-type and engineered viruses have been selected for targeting of specific cancers, to elicit cytotoxicity, and also to generate antitumor immunity. Conventional nonviral gene transfer systems include the direct tissue injection of DNA or transfection across the cell membrane using liposomes, peptide delivery systems, or polymer vectors[2]. One of them, DMBA-OC-1-TK+ was used to generate experimental ovarian cancer in 13 WKY female rats. In this work human ovarian epithelial cancer cell lines were infected with a recombinant adenoviral vector expressing the HSV-tk (AdRSV-tk) and were rendered sensitive to doses of GCV that were 100-200 times less than for untransfected cells. Our results demonstrate that HSVTK-modified mesothelial cells are sensitive to GCV killing in vitro and support the HSVTK bystander effect. Our data suggest that HPV pseudovirion may serve as a potential delivery vehicle for ovarian cancer gene therapy.

The results support the potential use of this approach as a gene therapy for OC, a disease that accounts for more deaths than any other cancer of the female reproductive system. There is also possible role of the roots in epithelial ovarian cancer which studies suggests that it can interfere with hormone receptor and neoplastic growth-related pathways through acting mechanisms. 1:20:51 – Has Dr. Intraperitoneal administration of HSVTK-expressing mesothelial cells in an established mouse model of ovarian cancer results in a statistically significant prolonged survival of treated animals. The gene products UL20, UL24, gK (UL53), and gB are termed modulators of cell fusion because mutations in any one of the four can confer the Syn phenotype (1, 3, 4, 13, 15, 23, 24, 31,42, 45, 46).

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