The most common form of kidney cancer among adults known as renal cell carcinoma seems to be a difficult to treat ailment. Scientists from the Virginia Commonwealth University Massey Cancer Center and the VCU Institute of Molecular Medicine (VIMM) have now designed a unique novel virus-based gene therapy for renal cell carcinoma. This treatment is apparently capable of destroying cancer cells at the primary tumor site and also in distant tumors that are not directly infected by the virus.
During the investigation, researchers tested the effectiveness of the medication Sorafenib (Nexavar) along with adenovirus (Ad.5/3-mda-7) for treating kidney cancer. It is known that adenoviruses infect the upper respiratory tract, but when employed for therapeutic purposes, the viruses seem to be beneficial. It appears that adenoviruses replace the harmful genetic material with genetic code, which activates biological processes in infected cells. At the time of the research, the Ad.5/3-mda-7 adenovirus was engineered to cause kidney cancer cells and normal cells protecting the kidneys for expressing the cancer-killing protein MDA-7/IL-24.
Paul Dent, Ph.D., Universal Corporation distinguished professor in cancer cell signaling at VCU Massey and vice chair of the department of neurosurgery, added, “While further research is needed, this therapy could be a novel and effective way to treat metastatic kidney cancer and prolong patient survival,” says Dent. “This is the first study to clearly define that gene therapeutic delivery of MDA-7/IL-24 in kidney cancer should be explored in the clinic, especially since we’ve demonstrated an established, FDA-approved drug enhances its toxicity to cancer cells.”
Mouse models were injected with the virus for triggering kidney cancer cells and making the normal cells line up kidneys for secreting the protein MDA-7/IL-24. Within the primary tumor site where the virus was first injected, the secreted MDA-7/IL-24 protein presumably halted tumor growth. As the protein entered the blood stream it seemingly stopped the growth of a second, distinct tumor not directly infected by the adenovirus. Such a result may be referred to as a ‘toxic bystander effect.’ It was mentioned that normal cells remained unaffected by the entire treatment procedure. Sorafenib apparently improves MDA-7/IL-24 toxicity in the laboratory and significantly elevates its anti-tumor effects in animal tumor models.
The research was published in the journal Cancer Biology and Therapy.