The aurora kinases are a group of serine threonine kinases associated with several cellular functions, including progression through mitosis, by regulating chromosome segregation, spindle formation and cytokinesis. The overexpression of aurora kinases has been reported in many human solid tumors, ultimately causing defects in centrosome purpose, aberrant spindle construction, misalignment of genetic instability, unusual cytokinesis and chromosomes, determining the activation of oncogenic pathways. Several authors reported an expression of the aurora A and B kinases also in leukemia cells, suggesting a possible role of these molecular targets in Icotinib the treatment of CML and ALL. Aurora kinase function is mediated by the phosphorylation of several substrates that have important roles in cell division, such as for example proteins survivin, CENP An and serine 10 on histone H3. The aurora kinases range in size from 309 to 403 proteins. They’ve a C terminal domain that’s accountable for regulation of the protein levels via proteasomal Lymph node degradation, a highly conserved catalytic domain, and a brief N terminal domain that varies in length between the kinases and plays a role in the different locations of the kinases within cells. The aurora An isotype is widely expressed in growing normal cells, with expression being cell cycle dependent and peaking at the point of the cell cycle. All through mitosis, the kinase is almost restricted to the spindle poles, where it is needed for centrosome separation and maturation. An overexpression of aurora A causes an increase in aneuploidy and centrosome numbers, leading to the transformation of mammalian cells and also causes resistance to apoptosis induced by taxol in human cancer cell lines. Moreover, this kinase is a key regulatory component of the p53 pathway as its overexpression leads to increased p53 destruction, which facilitates oncogenic transformation. Individual aurora An is proposed as a drugable target in a number of tumors including pancreatic, hepatocellular, breast, nonendometriod, and ovarian carcinomas,51 gliomas and hostile non Hodgkins lymphoma. Aurora T activity is required for condensation and bipolar chromosome direction. Aurora T kinases are genetic traveler proteins, which are located map kinase inhibitor in cells in a complex with survivin and inner centromere protein. The over-expression of an aurora B kinase dead mutant causes numerous defects in the mitotic machinery, including the lack of kinetochore attachment to microtubules and the exit from mitosis without anaphase or cytokinesis. Aurora D over-expression is detected in tumor cell lines in vitro60 and in biopsy samples from colorectal carcinoma.