study give a new understanding on the role played from the IN flexible trap during drug response and the integration process. Future structural studies may be guided by these results to better model the IN active site and enable the development of next-generation IN inhibitors to overcome RAL resistance. MicroRNAs act in the post transcriptional level to regulate gene expression in almost histone deacetylase inhibitors every natural process, including oncogenesis. Here we report the identification of a group of miRNAs which can be differentially regulated in childhood adrenocortical tumors, including miR 99a and miR 100. Functional analysis of those miRNAs in adrenocortical tumor cell lines showed that they coordinately regulate expression of the IGF mTOR raptor signalling path through binding web sites in their UTRs. In these cells, the energetic Ser2448 phosphorylated form of mTOR occurs only substitution reaction in mitotic cells in colaboration with the mitotic spindle and midbody in the stages of the cell cycle. Pharmacological inhibition of mTOR signalling by everolimus considerably reduces tumor cell growth in vitro and in vivo. Adrenocortical tumors in children might occur sporadically or in association with other styles of neoplasms in the context of multiple neoplasia syndromes connected to germline tumor suppressor gene mutations. The occurrence of these tumors is highest during the first three years of life and is many times more frequent in southern Brazil than in the relaxation of the world. Because geographic location, youth ACT are nearly invariably linked to the germline R337H cyst protein p53 mutation. These tumors are believed to be based on the fetal adrenal due to their age distribution, their sample of hormone secretion and their molecular phenotype. Whilst the most frequent genetic basis of childhood deubiquitinating enzyme inhibitors ACT are germline TP53 mutations with loss of heterozygosity in the tumefaction, our understanding of the molecular pathogenesis of those neoplasms remains limited. IGF2 signalling through the IGF 1R is considered to represent a significant mechanism for ACT development and a relevant therapeutic target. In addition, amplification and over-expression of the nuclear receptor Steroidogenic Factor 1 is thought to play an essential part in ACT pathogenesis. Last, research of protein coding mRNAs found a definite pattern of the expression in childhood ACT compared to typical adrenal cortex and also identified a set of transcripts whose expression relates to prognosis.