As recommended by the maker, total RNA was transcribed to cDNA using the RevertAid H Minus M uLV Reverse Transcriptase set. Finally, all samples were normalized to 700 ng/ul so that PCRs were performed with similar amounts of total cDNA. GAPDH was used as internal control because physical expression in the neonatal rat lumbar spinal-cord. Each PCR contained: 1 ul of cDNA, 2 ul of 10 PCR buffer, 2. 0 mM MgCl2, 0. 2 mM dNTPs, 1. 0 ul of each primer and 2. 5 U of Taq DNA polymerase. Amplification system was executed as follows: preliminary denaturation for 5min at 94 C, repeated cycles of denaturation for 30 s at 94 C, annealing for 45 s at 59 C, 58 C or 63 C, extension for 1 min at 72 C and ultimate extension for 7 min at 72 C. Number of PCR cycles for every primer set was plumped for in the linear amplification angiogenesis in vitro variety determined by plotting the optical density of the PCR products versus number of cycles, as previously described. Therefore, amplification was performed with 29 or 32 rounds. Expected size for PCR services and products was: 361 bp, 612 bp and 306 bp. The amplified fragments were subjected to electrophoresis in 1% agarose gel and discovered by ethidium bromide staining. Ties in were visualized under UV light and photographed. Optical densities of the groups were determined by using the Image Master VDS application. The ratio between your optical density of the GAPDH band and band for every sample was thought as optical density ratio. Neuroblastoma is a pediatric extracranial cyst Plastid that demonstrates complex clinical and biological heterogeneity. It is a growth of the sympathetic nervous system and it originates mostly in adrenal gland and also in chest, throat, stomach, and pelvis. Using aggressivemultimodal treatment such as stem cell transplantation, surgery, light, and che motherapy, the success rate of kiddies more than 18 months is very low because of poor reaction to conventional treatment methods. Therefore, development of novel therapeutic strategy is urgently required for treatment of neuroblastoma in infants. Neuroblastoma is usually associated with overexpression of oncogenic success factors and resistance to chemotherapy. The anti apoptotic Bcl 2 protein prevents apoptosis and keeps cellular homeostasis. Bcl 2 mediated inhibition of chemotherapy in neuroblastoma has previously been described. The molecular mechanism by which Hedgehog inhibitor Bcl 2 performs its anti apoptotic features is considered to be due to blockage of mitochondrial pathway of apoptosis. Hence, targeting anti apoptotic functions of Bcl 2 is actually a possible strategy for treatment of neuroblastoma. We used a small particle Bcl 2 inhibitor named HA14 1, which fits into hydrophobic cleft of Bcl 2 protein and disturbs its antiapoptotic features. HA14 1 induces apoptosis due to inhibition of Bcl 2 interaction and binding with pro apoptotic Bax in glioblastoma cells.