Oncoapoptosis: a novel molecular therapeutic for cancer treatment.
Many cancer cells refractory to radiation treatment and chemotherapy proliferate due to loss of intrinsic programmed cell death (apoptosis) regulation. Consequently, the resolution of these cancers are many times outside the management capabilities of conventional therapeutics. We have developed a replication defective herpes simplex virus system which triggers apoptosis specifically in transformed human cells, termed oncoapoptosis. Susceptibility to virus induced cell death is dependent on the p53 protein status in the tumor cells, indicating specific targeting of the treatment. Primary cells which produce functional p53 are resistant to oncoapoptotic killing but not to apoptosis induced by nonviral environmental factors. Thus, induction of apoptosis by nonreplicating virus is a feasible molecular therapeutic approach for killing human cancer cells. Our findings have important implications in designing novel virus-based anticancer strategies.
Blaho
John A
JA
Department of Microbiology, Mount Sinai School of Medicine, NY 10029-6574, USA. john.blaho@mssm.edu
D017209:Apoptosis / Q000235:genetics*; D045744:Cell Line, Tumor; D015316:Genetic Therapy; D006367:HeLa Cells; D006801:Humans; D009369:Neoplasms / Q000628:therapy*; D018139:Simplexvirus / Q000235:genetics* / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D014779:Virus Replication / Q000235:genetics
D016159:Tumor Suppressor Protein p53