The CDKN2A acts as a cyclin-dependent kinase inbibitor, inbibitin

The CDKN2A acts as a cyclin-dependent kinase inbibitor, inbibiting the binding of the CDK4 selleck chemicals 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 OSI-906 purchase 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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