Unit 377, Houston, TX 77030, Phone: 1794 3201 Fax: 1563 9952, JEWoolerymdanderson Daruka Mahadevan, MD, Ph.D, Associate Professor of Medicine, Division of Hematology H / Oncology, Arizona Cancer Center in Tucson, the development of drugs AZ, director and director of translational research, the Phase I program, mailing address: 3838 N. Campbell Ave, CCT128930 885499-61-6 Tucson, AZ 85719, Phone: 1694 0191, Fax: 1626 2225 tion dmahadevanazcc.arizona explanation of interest The authors state financial assistance in the form of the spore’s lymphoma grant from the National Institutes of Health and the National Cancer Institute . The authors explained Ren, they have no other Ver Ffentlichung. NIH Public Access Author Manuscript Expert Opin Drug Discov. Author manuscript, increases available in PMC 2012 1 M rz.
Ver published in its final form: Expert Opin Drug Discov. M March 2011, Clinofibrate RAAS inhibitor 6: 291,307th doi: 10.1517/17460441.2011.555395. PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript NIH Keywords mitosis, assembly of centrosomes, Aurora kinase inhibitor, small molecule inhibitors, targeted cancer therapy, controlled station The mounting pin that aneuplo 1.0 Introduction br attract die of cancer on humanity without parallel, is already achieved the distinction of being the leading cause of death and economic burden world.1, 2 is a cancer characterized by uncontrolled proliferation EAA leads to a malignant Ph Genotype. Mitosis is a critical step in cancer cell proliferation and has many redundant systems and control point The contr Lant important steps in the process.
The Aurora kinase family play an R Important in maintaining the fidelity of mitosis. This is the theory that the anti-cancer benefits may be derived from inhibition of Aurora kinase activity of t, leading to the development of several Aurora kinase inhibitors operate. 1.1 The Aurora kinase Aurora kinases are a family of oncogenic serine / threonine kinases involved in mitotic phase of the cell cycle, acting to maintain the mitotic spindle to establish bipolar spindle formation, the orientation of the mitotic spindle to centrosomes, the centrosome separation, mitosis and cytokinesis followed checkpoint.3 are 4,5,6 Aurora kinases essential for accurate chromosome division and organized for each daughter cell. In addition, Aurora kinases are frequently in tumor cells that overexpressed particularly those with high growth fractions.
There are three known Aurora kinases in human tissues and non-neoplastic neoplastic. Aurora kinases A and B are expressed in all tissues in the world, w While Aurora-C kinase is predominantly expressed in the testis, to participate in meiosis. But recent research has Aurora kinase C activity of t with tumor formation in somatic tissues and perhaps cancer relevant target.3, 7,8 All three Aurora kinases have significant sequence and structural homology and overlapping gene expression in conjunction with catalytic Dom ne, genomic L length and kinase activity of t, although the cellular other functions and end portions of each differ.9 N, 10 Inhibition of Aurora kinase activity of t leads to catastrophic failure mitosis, such as M deficiencies in of cytokinesis, centrosomes misaligned, and malformation of the mitotic spindle that their H are hepunkt in apoptosis.
10, 11 different compounds in the development of capital from the anti-cancer effects of inhibition of Aurora kinase activity of t. 1.2 Relevance of Aurora A kinase Aurora-A kinase is h Frequently in many epithelial tumors, cancers and tumors of solid organs verst RKT. Aurora A kinase has an impact