The CDKN2A acts as a cyclin-dependent kinase inbibitor, inbibiting the binding of the CDK4 protein to cylclin D1 and thus preventing phosphorylation of the Rb protein and arresting the cell cycle in the G1phase [18, 19]. Cyclin D1 overexpression, CDKN2A loss, and pRb inactivation play a key role in glioma tumorigenesis [20–22]. The results indicated that overexpression CDKN2A has the potential to be developed into a future

treatment for glioma patients. Conclusions Our study suggests that CDKN2A as a malignant gliomas suppressor gene, appears to be useful for predicting behaviour of high-grade malignant gliomas. CDKN2A-Cyclin-Rb pathway plays a key role on malignant gliomas formation and that therapeutic targeting of this pathway may be useful in malignant gliomas treatment. References 1. Ohgaki H, Kleihues P: Epidemiology www.selleckchem.com/products/EX-527.html and etiology of gliomas. Acta Neuropathol 2005, 109:93–108.PubMedCrossRef 2. Rasheed BK, Wiltshire RN, Bigner SH, Bigner DD: Molecular pathogenesis of malignant gliomas. Curr Opin Oncol 1999, 11:162–167.PubMedCrossRef 3. Bigner SH, Mark J, Burger PC, Mahaley MS Jr, Bullard DE, Muhlbaier LH, Bigner

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