Mitogenic signaling cascades in glial tumors

Neurosurgery. 2003 Jun;52(6):1425-34; discussion 1434-5. doi: 10.1227/01.neu.0000065135.28143.39.


Gliomas are primary central nervous system tumors that arise from astrocytes, oligodendrocytes, or their precursors. Gliomas can be classified into several groups according to histological features. A number of genetic alterations have been identified in human gliomas; these generally affect either signal transduction pathways activated by receptor tyrosine kinases or cell cycle growth arrest pathways. These observed genetic alterations are now being used to complement histopathological diagnosis. The aim of the present review is to give a broad overview of the receptor tyrosine kinase signaling machinery involved in gliomagenesis, with an emphasis on the cooperative interaction between receptor tyrosine kinase signaling and the cell cycle-regulatory machinery. Understanding molecular features of primary glial tumors will eventually allow for target-selective intervention in distinct glioma subsets and a more rational approach to adjuvant therapies for these refractory diseases.

Publication types

  • Review

MeSH terms

  • Adult
  • Brain Neoplasms / physiopathology*
  • Epidermal Growth Factor / physiology
  • ErbB Receptors / physiology
  • Glioma / physiopathology*
  • Humans
  • MAP Kinase Signaling System / physiology*
  • Platelet-Derived Growth Factor / physiology
  • Receptor Protein-Tyrosine Kinases / physiology
  • Receptors, Platelet-Derived Growth Factor / physiology


  • Platelet-Derived Growth Factor
  • Epidermal Growth Factor
  • ErbB Receptors
  • Receptor Protein-Tyrosine Kinases
  • Receptors, Platelet-Derived Growth Factor