Such vectors have already been documented to be safe for human use. Alternative viruses with single or less-attenuating mutations demonstrate greater oncolytic capacity are also already in clinical trials. Coupling this screening strategy to less attenuated viruses will likely diversify its utility among the various solid malignancies as well as enhance the therapeutic component. Agents that are simultaneously both diagnostic and therapeutic have been dubbed ����theragnostic.���� It is possible our strategy could be Kojic acid further refined by the use of a more robust cancer-dependent promoter to drive biomarker expression. Improved vector delivery to the tumor may also be achieved using tumor targeting small molecule and nanoparticles uptake-enhancement strategies as recently described with the use of internalizing RGD peptides. Eventual commercialization of our proposed screening strategy would EF-24 benefit from using biomarkers that are already in widespread use such as bHCG, PSA and aFP. Biomarker assay sensitivity in the context of this screening strategy can still improve exponentially as is being realized with microfluidic technologies. A significant concern for the prototypical cancer screening method developed in this work is the development of an immune response to the gene delivery agent or the transduced biomarker that would preclude repeated use of the screening tool. Previous work in the field has shown that pre-immunized animals still experience therapeutic benefit from HSV with sustained efficacy. Because 80% of the general population has been exposed to HSV, implementing this detection strategy with HSV will depend upon the efficacy of engineered HSVs administered to immunocompetent subjects who have previously been exposed to wild-type HSV strains. In vitro screening for mouse tumor cell lines revealed that all mouse lines we tested exhibited comparably low susceptibility to infection by our attenuated mutant virus, on par with normal quiescent human cells. In vivo models of HGF116 demonstrated no virus sensitivity following i.t. or i.v. injection. Thus, we are unable to assess our cancer screening strategy in an immunocompetent model until the identification of mouse models that are more susceptible to human HSV.