Glioblastoma is a highly aggressive form of brain cancer characterized by uncontrolled cell growth resulting from a loss of cell cycle regulation. In this study we determined the antiproliferative eects of interferon gamma (IFNg) on the glioblastoma cell lines T98G, SNB-19 and U-373, focusing on the ability of IFNg to increase levels of p21, an important negative regulator of cell cycle events. IFNg was found to inhibit the growth of all cell lines, with inhibition ranging from 82.2% to 45.4%. Flow cytometry analysis showed that IFNg treatment caused a cell cycle delay in the G 1 or S phases. The strength of this delay varied, correlating with the degree by which IFNg inhibited proliferation of each cell line. IFNg treatment increased the production of the cyclin dependent kinase inhibitor (CKI) p21 /cyclin-dependent kinase 2 (cdk2)/cyclin showed that the amount of p21 WAF1/CIP1 in the complexes and the inhibition of cdk2-cyclin kinase activity correlated with the level of p21 WAF1/CIP1 produced in the cells by IFNg. These results show that IFNg has signi®cant antiproliferative eects on the glioblastoma cell lines and suggest that p21 WAF1/CIP1 plays a role in mediating these eects.

PMTCT interventions, including sdNVP, are working in program settings. However, postnatal transmission especially after 6 months through suboptimal feeding practises remains an important challenge to further reduce pediatric HIV.