Vaccinia virus-mediated expression of wild-type p53 suppresses glioma cell growth and induces apoptosis.

Immunogenicity and Safety of Defective Vaccinia Virus Lister: Comparison with Modified Vaccinia Virus Ankara

“…The recombinant p53-expressing viruses induced CPE in almost every cell line at concentrations 1 order of magnitude lower. A likely explanation is that overexpression of the p53 gene additionally induces apoptosis, as was seen for replicating vaccinia viruses (42). In summary, the nonreplicating viruses were less virulent in cell culture, inducing a CPE at doses 5 orders of magnitude higher than those of the wild-type strain, and should therefore be safer in animals.…”

Eradication of Solid Human Breast Tumors in Nude Mice with an Intravenously Injected Light-Emitting Oncolytic Vaccinia Virus

“…Intraperitoneal delivery of the TK À and VGF À viral strain shows growth retardation of tumors in mice (19). Additionally, foreign genes encoding tumor suppressor proteins, immunostimulatory proteins, and cytokines, as well as pro-drug-activating enzymes, have been inserted into the nonessential loci of VACV genome for therapy of tumors (21)(22)(23).…”

Astrocyte-specific expression of CDK4 is not sufficient for tumor formation, but cooperates with p53 heterozygosity to provide a growth advantage for astrocytes in vivo

“…In the primary GFAP-hCDK4 astrocyte cultures, the lack of a cell autonomous growth advantage re¯ects the inability of CDK4 overexpression by itself to signi®cantly accelerate cell proliferation in the absence of additional growth regulatory pathway alterations present in the C6 glioma cells. C6 glioma cells harbor alterations in p53 function, including p53 mutation and a decrease in wild-type p53 expression (Yin et al, 1995;Scotto et al, 1998;Timiryasova et al, 1999) as well as RAS pathway activation (Guha et al, 1997) and therefore exhibit changes associated with human astrocytoma formation. In contrast, there is little evidence for Rb pathway dysfunction in C6 cells.…”