Schwannomas are benign tumors forming along peripheral nerves that can cause deafness, pain and paralysis. Current treatment involves surgical resection, which can damage associated nerves. To achieve tumor regression without damage to nerve fibers, we generated an HSV amplicon vector in which the apoptosis-inducing enzyme, caspase-1 (ICE), was placed under the Schwann cell-specific P0 promoter. Infection of schwannoma, neuroblastoma and fibroblastic cells in culture with ICE under the P0 promoter showed selective toxicity to schwannoma cells, while ICE under a constitutive promoter was toxic to all cell types. After direct intratumoral injection of the P0-ICE amplicon vector, we achieved marked regression of schwannoma tumors in an experimental xenograft mouse model. Injection of this amplicon vector into the sciatic nerve produced no apparent injury to the associated dorsal root ganglia neurons or myelinated nerve fibers. The P0-ICE amplicon vector provides a potential means of 'knifeless resection' of schwannoma tumors by injection of the vector into the tumor with low risk of damage to associated nerve fibers.

Human cytomegalovirus (HCMV) has many strategies to survive the attack of the host. HCMV infection of host cells induces cellular activation and disturbance of the cell cycle. It is possible that HCMV modulates the behavior of certain cancer cells that are susceptible to HCMV infection. This study was performed to identify the possible mechanism of resistance to apoptotic stimuli in some cancer cell lines by HCMV infection. HCMV‐infected cancer cells showed resistance to apoptosis induced by the topoisomerase II inhibitor etoposide. UMG1–2, which constitutively expresses HCMV immediate‐early protein‐1 (IE1), had resistance to apoptosis induced by etoposide as compared with the parental cell line U373MG. Measurement of caspases activity with fluorogenic substrates in etoposide‐treated U373MG and UMG1–2 cells and the direct activation of caspase‐3 with peptides containing arginine‐glycine‐aspartate in U373MG and UMG1–2 cells revealed that the inhibition level of apoptosis by HCMV IE1 would be upstream of caspase‐3 in the caspase cascade pathway. Cellular expression of Cdk2 was increased in UMG1–2 after etoposide treatment while the expression of E2F‐1 in UMG1–2 was decreased as compared with that in U373MG. The Cdk2 inhibitor, roscovitine, decreased the resistance to apoptosis on etoposide‐treated UMG1–2. These results suggest that aberrant HCMV infection confers resistance to anticancer drugs on some cancer cells and protects cells from apoptosis, possibly due to the deregulation of cyclin‐dependent kinase by HCMV immediate‐early protein.

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We have investigated an effective and a single-step chemical vapor deposition (CVD) method to achieve conformal visible poly-dichloro-para-xylylene (parylene C) film for light extraction enhancement in bottom-emitting organic light-emitting diodes (OLEDs) at room temperature. We report that sublimed parylene dimers pyrolyzed between 400 °C and 500 °C resulted in visible parylene films with tunable transmittance and haze, exhibiting light scattering properties due to the formation of uniformly distributed dimer crystals. We achieved a novel conformal visible parylene film with total transmittance and high haze of 79.5% and 93.6%, respectively. It is observed that the outcoupling efficiency of the OLEDs employing the visible parylene film is enhanced up to 45.8%. Additionally, the OLED with the visible parylene light extraction film shows limited angle-dependency of emission spectrum over viewing angles. The single-step room temperature fabrication process of this conformal outcoupling film paves the way to achieving commercial high-performance OLEDs.