Future treatment modalities for meningiomas - Targeting of neurofibromatosis type 2 and Ras-regulated pathways

The loss of neurofibromatosis type 2 (NF2) tumor suppressor gene function a nd enhanced proliferative signal transduction through the Ras pathway are t he hallmark of meningioma tumorigenesis. Although the exact mechanisms by w hich NF2 and Ras proteins contribute to meningioma tumorigenesis remain to be elucidated, the present knowledge is sufficient to start exploring excit ing therapies that are directed at these molecular targets. Gene therapy to restore the functions of inactivated NF2 tumor suppressor protein and the use of several promising agents that target signal transduction molecules o f the Ras pathway are reviewed. An increased understanding of the biologic functions of the new therapeutic targets discussed in this article will fac ilitate the development of meningioma treatments that are minimally toxic, yet highly effective.