The Aurora serine threonine protein kinases really are a group of three kinases with various tissue and temporal expression profiles that play critical roles in meiosis and mitosis, defects in which can cause apoptosis induction and excessive mitotic functions. The essential character of Aurora Icotinib kinase An is outlined by the fact genetically engineered null mice are embryonic lethal. Aurora kinase An activity can be needed for spindle checkpoint formation and separation, microtubule kinetochore attachment, centrosome duplication, cytokinesis, the G2/M transition, and phosphorylation of Polo like kinase 1. More, Aurora kinase An is implicated as an oncogenic driver in human cancers. Aurora kinase A has been observed to be overexpressed in cancer cells, and the AURKA gene locus is amplified in selected adult tumors. Aurora kinase inhibitors with different specificities and activities as well as pharmacodynamic markers are currently being evaluated, and some are already well high level in clinical studies. These types of inhibitors show a broad range of activity, with AZD 1152 becoming an example Inguinal canal of a selective Aurora kinase B inhibitor and MLN8054 an example of a selective Aurora kinase An inhibitor. The effects of Aurora kinase An inhibition are numerous, as corresponds to the assorted nature of its substrates, and include abnormal spindle post creation, expansion reduction, and polyploidy, followed by apoptosis induction. The latter can involve signaling mediated by p53, as Aurora kinase A has been shown to modify the phosphorylation status of p53 and histone H3 and to communicate with the MYCN protein, limiting p53 ubiquitination and degradation by the proteasome in neuroblastoma cell lines. Although p53 is generally non functional in cancer cells, inhibition of Aurora kinase A by MLN8054 can lead to p73 dependent Cabozantinib clinical trial apoptosis in p53 deficient cells. Aurora kinase A has also been reported to influence cell survival through the Akt pathway and by interfering with IkBa. The primary focus of the Pediatric Preclinical Testing Program is to identify novel agents which have significant antitumor activity against acute lymphoblastic leukemia and types of childhood solid tumors as you source of data to use in prioritizing clinical progress of such agents in the pediatric setting. The PPTP has described the single representative evaluation of action of the Aurora kinase An inhibitor MLN8237 against its panels of in vitro cell lines and in vivo xenograft models. The neuroblastoma and ALL sections were particularly sensitive to the single agent treatment. In fact, this Aurora kinase An inhibitor may be the only drug out of over 20 examined with preferential activity contrary to the neuroblastoma panel.