New insights into meningioma: from genetics to trials

Curr Opin Oncol. 2012 Nov;24(6):660-5. doi: 10.1097/CCO.0b013e3283571a06.

Abstract

Purpose of review: In view of growing interest and need for nonsurgical therapies of meningiomas, we reviewed relevant articles published in the period from December 2010 to April 2012.

Recent findings: Large population-based, case-control studies have resulted in identification of new etiology factors, such as smoking or allergy, as well as new genes shown to play a role in meningioma susceptibility. Although aggressive surgery is still the treatment of choice for meningioma patients, even in the elderly population, postoperative radiotherapy remains debated and limited to Grade II residual cases as well as Grade III tumors. Although preclinical studies have pinpointed new candidate drugs to stop meningioma growth, such as trabectedin and histone deacetylase inhibitors, there are currently no effective therapies for meningiomas. Several clinical trials are under way, mostly on heavily pretreated patients, to determine the efficacy of some of the most promising candidate drugs, platelet-derived growth factor receptor-targeted therapies, and antiangiogenetic drugs being on the top list. Robust genetically engineered mouse models should be used as 'filters' to select agents for human clinical trials.

Summary: Surgical approach combined with radiotherapy in selected cases remains the most appropriate for meningioma patients. New therapies are under investigation and should modify treatment paradigms in the future.

Publication types

  • Review

MeSH terms

  • Animals
  • Case-Control Studies
  • Chromosomal Proteins, Non-Histone / genetics
  • Clinical Trials as Topic
  • DNA-Binding Proteins / genetics
  • Genes, Neurofibromatosis 2
  • Genetic Association Studies
  • Humans
  • Meningeal Neoplasms / blood supply
  • Meningeal Neoplasms / genetics*
  • Meningeal Neoplasms / therapy*
  • Meningioma / blood supply
  • Meningioma / genetics*
  • Meningioma / therapy*
  • Mutation
  • Neoplasm Recurrence, Local / prevention & control
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / prevention & control
  • Risk Factors
  • SMARCB1 Protein
  • Transcription Factors / genetics

Substances

  • Chromosomal Proteins, Non-Histone
  • DNA-Binding Proteins
  • SMARCB1 Protein
  • SMARCB1 protein, human
  • Transcription Factors