Brain and spinal tumors are the second most common malignancies in childhood after leukemia, and they remain the leading cause of death from childhood cancer. The role of autophagy, a catabolic cellular process used to provide energy during times of stress, in pediatric tumors is unknown. Here we present studies done in pediatric medulloblastoma cell lines (DAOY, ONS76) and atypical teratoid/rhabdoid tumor cell lines (BT-16, BT-12) to test this role. Autophagy was inhibited using siRNA against autophagy related genes ATG12 and ATG7 or pharmacologically induced using rapamyacin or inhibited using chloroquine to test the effect of autophagy on chemosensitivity. We found that when pediatric brain tumor cells are under starvation stress or exposed to known autophagy inducers, they show increased levels of autophagy. We also found that current chemotherapeutics (CCNU, cisplatin) stimulate autophagy in pediatric brain cancer cells. Silencing of ATG12 and ATG7 prevents this increase and autophagy can be pharmacologically stimulated and inhibited. Although autophagy can be induced and inhibited in these cell lines, the effect of autophagy on tumor cell killing is small. This may have significant clinical relevance in the future planning of therapeutic regimens for pediatric brain tumors.