Abstract
Meningiomas are by far the most common tumors arising from the meninges. A myriad of aberrant signaling pathways involved with meningioma tumorigenesis, have been discovered. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. An understanding of the genetic and molecular profile of meningioma would provide a valuable first step towards developing more effective treatments for this intracranial tumor. Chromosomes 1, 10, 14, 22, their associated genes, and other potential targets have been linked to meningioma proliferation and progression. It is presumed that through an understanding of these genetic factors, more educated meningioma treatment techniques can be implemented. Future therapies will include combinations of targeted molecular agents including gene therapy, si-RNA mediation, proton therapy, and other approaches as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas. This review provides an overview of the current knowledge of the genetic, signaling and molecular profile of meningioma and possible treatments strategies associated with such profiles.
Highlights
Menigiomas are the second-most common central nervous system tumor in adults [1,2,3,4]
When the NF2 gene is mutated, merlin production is impaired that leads to an increase of Yes-associated protein (YAP) levels in the CNS that can lead to meningioma proliferation
Numerous pathways have been linked to meningioma proliferation and progression [4], which get activated by the many genetic factors that lead to these tumors (Figure 2)
Summary
Menigiomas are the second-most common central nervous system tumor in adults [1,2,3,4]. Many genetic factors and pathways have been linked to the proliferation, tumorgenesis, progression, and recurrence of meningiomas. The NF2 gene codes for the protein merlin that acts as a tumor suppressor for many different cell types.
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