This is the first study assessing viral miRNAs in SEOC. In this study, Balveen Kaur, PhD, professor of neurological surgery at the Ohio State University Comprehensive Cancer Center, and colleagues tested the antitumor efficacy of 34.5ENVE in a series of ovarian cancer cell lines, mouse tumor cells, and human tumor cells. Solove Research Institute (OSUCCC–James), led the cell and animal study. Our preliminary studies suggest that HSV-1 may be a promising alternative vector for ovarian cancer gene therapy. Fu et al., Mol. HSV-G207 infected both EOC cells and mesothelial cells; however, unlike EOC cells, mesothelial cells provided a poor substrate for replication of HSV-G207. Methods To identify microRNA of interest, microRNA expression profiling was performed on 4 SEOC cell lines and normal human ovarian surface epithelial cells.
The node sizes indicated the significance of association between the genes with cancer survival. This was accompanied by a significant increase in the number of tumor-associated NK and CD8+ T cells expressing CXCR3 and CD25. The mixture was serially diluted and then used to infect Vero cell monolayers. Five patients underwent second-look surgery about one month after gene therapy (GT). Further more, all of the HSV-tkc positive clones exposed to 10 micrograms/ml GCV could be eliminated, and 96% of those clones died in 5 days after GCV was used. We also administered interleukin−12-expressing oncolytic herpes simplex virus to the peritoneal cavity of mice that had developed spontaneous, metastatic ovarian cancer and determined overall survival and tumor burden at 95 days. This system is well characterized, and has been widely used in different gene-therapy based strategies.
We also administered interleukin-12-expressing oncolytic herpes simplex virus to the peritoneal cavity of mice that had developed spontaneous, metastatic ovarian cancer and determined overall survival and tumor burden at 95 days. Stromal cells can stimulate the growth of tumor cells. In particular, replication-competent recombinant HSV strains may offer distinct advantages in oncolytic therapy of epithelial tumors: (a) HSV is highly infectious to tumors of epithelial origin, resulting in high efficacy (70); (b) there is considerable redundancy in HSV receptors, which makes the loss of HSV receptors by tumors due to mutations less likely; (c) antiherpetic drugs are commercially available, which may be used clinically to control undesired side effects, should local or systemic spread of the virus occur; and (d) because of its large genome, HSV offers ample packaging opportunities – up to 30 kb – without affecting viral replication in cancer cells. Similarly, chemotherapy-sensitive ovarian cancer cells A2780 and PA-1, possessing wild-type p53, and their respective chemotherapy-resistant clones A2780/200CP, lacking p53 function, and PA-1/E6, permanently expressing the HPV E6 gene, were equally sensitive to HSV oncolysis. Our preliminary studies suggest that HSV-1 may be a promising alternative vector for ovarian cancer gene therapy. Tissue response was evaluated. We therefore devoted the second year of this project to evaluate the toxicity of Synco-2D.
Other possible vector-associated constitutional symptoms, abdominal pain, and gastrointestinal symptoms were experienced by 6 of 14 (43%) treated patients. Fu et al., Mol. An HSV-1 mutant, hrR3, has replaced the gene encoding ribonucleotide reductase (RR) with the lacZ reporter gene. In the current study, we explore the use of a human papillomavirus (HPV) pseudovirion to deliver a herpes simplex virus thymidine kinase (HSV-tk) gene to ovarian tumor cells. HF10 injection prolonged survival and decreased intraperitoneal dissemination, but to a lesser extent than the mGM-CSF amplicon. HF10 injection prolonged survival and decreased intraperitoneal dissemination, but to a lesser extent than the mGM-CSF amplicon. The OVs that are currently being developed to treat ovarian cancer are summarized in .
With the continuous development of molecular biology, gene therapy for OC has become a notable field of study (5). Solove Research Institute (OSUCCC – James), led the cell and animal study. Carroll, Mark A. TNFα expression under the CMV or US11 promoter was compared on cell lines CT26, BHK and Fadu. As a proof of concept, we genetically engineered mesothelial with the herpes simplex virus thymidine kinase/ganciclovir (HSVTK/GCV) system to deliver cytotoxicity to human ovarian cancer cells. Levy, and NURSE COORDINATOR: Kay J. The TK or IL-2 expression was permanent in OVHM/TK or OVHM/IL-2.
We found that transfection of DNA from KOS-804, a previously described HSV-1 syncytial (Syn) strain whose Syn mutation was mapped to an amino acid substitution in gK, induced numerous large syncytia on HveA-expressing Chinese hamster ovary cells (CHO-HVEM12) but not on control cells (CHO-C8). Background: HSV1790 is an oncolytic virus generated by inserting the enzyme nitroreductase (NTR) into the virus HSV1716. Two-thirds of women present with progressive disease wherein the cancer has already disseminated to abdominal organs or distant sites (1). This article has been cited by other articles in PMC. BACKGROUND: This study evaluated the potential of gene therapy against ovarian cancer usin the retroviral transfer of the herpes simplex type 1 thymidine kinase gene (HSV1-TK) followed by ganciclovir treatment.