Use of an oncolytic vaccinia virus for the treatment of canine breast cancer in nude mice: preclinical development of a therapeutic agent.

Mammary cancers together with cancers of the skin account for about 60% of the total cancers occurring in dogs. The veterinary options for therapeutic management of canine mammary cancer are limited and prognosis for such patients is poor. In this study, we analyzed the functionality of the oncolytic vaccinia virus strain GLV-1h68 as a possible therapeutic agent for canine mammary cancer.

Primary naive and interleukin-2-activated natural killer cells do not support efficient ectromelia virus replication.

Natural killer (NK) cells are known for their ability to lyse tumour cell targets. Studies of infections by a number of viruses, including poxviruses and herpesviruses, have demonstrated that NK cells are vital for recovery from these infections. Little is known of the ability of viruses to infect and complete a productive replication cycle within NK cells.

Establishment and characterization of conditions required for tumor colonization by intravenously delivered bacteria.

Intravenously injected bacteria have the ability to enter and replicate within tumors in mice. Here, we further characterized this dynamic process by investigating the conditions required for tumor colonization by bacteria. We discovered that a broad range of bacteria, including both Gram-negative and Gram-positive strains, colonize a panel of syngeneic and xenogeneic tumors, as well as spontaneous tumors in mice.

Eradication of solid human breast tumors in nude mice with an intravenously injected light-emitting oncolytic vaccinia virus.

Previously, we reported that a recombinant vaccinia virus (VACV) carrying a light-emitting fusion gene enters, replicates in, and reveals the locations of tumors in mice. A new recombinant VACV, GLV-1h68, as a simultaneous diagnostic and therapeutic agent, was constructed by inserting three expression cassettes (encoding Renilla luciferase-Aequorea green fluorescent protein fusion, beta-galactosidase, and beta-glucuronidase) into the F14.5L, J2R (encoding thymidine kinase) and A56R (encoding hemagglutinin) loci of the viral genome, respectively.