Correlation of molecular genetic analysis of p53, MDM2, p16, PTEN, and EGFR and survival of patients with anaplastic astrocytoma and glioblastoma

Front Biosci. 2003 May 1:8:e281-8. doi: 10.2741/865.

Abstract

This article reviews studies on the correlation between genetic abnormalities in malignant astrocytic tumors and patient survival. It is almost certain that alterations of PTEN on chromosome 10 represent a significant unfavorable prognostic factor in glioblastoma patients. The association of alterations in p53, MDM2, p16 or EGFR with the survival of patients with anaplastic astrocytoma or glioblastoma remains controversial. It is possible that the p16 alteration and EGFR amplification are associated with poor survival in certain groups of patients and that there might be a relationship with age. Malignant transformation of astrocytic cells are driven by the sequential acquisition of genetic alteration. Therefore, it is reasonable to subgroup gliomas by their patterns of genetic alterations. However the studies that correlated the multiple genetic alterations with survival are still limited. Further studies on large cohorts are necessary to elucidate the genetic factors that affect the prognosis and response to therapy of patients with malignant gliomas and to develop effective management strategies.

Publication types

  • Review

MeSH terms

  • Astrocytoma / genetics*
  • Astrocytoma / mortality*
  • Central Nervous System Neoplasms / genetics*
  • Central Nervous System Neoplasms / mortality*
  • Genes, Tumor Suppressor*
  • Genes, erbB-1*
  • Genes, p16
  • Genes, p53
  • Glioblastoma / genetics
  • Glioblastoma / mortality
  • Humans
  • Nuclear Proteins*
  • PTEN Phosphohydrolase
  • Phosphoric Monoester Hydrolases / genetics*
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-mdm2
  • Tumor Suppressor Proteins / genetics*

Substances

  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Tumor Suppressor Proteins
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2
  • Phosphoric Monoester Hydrolases
  • PTEN Phosphohydrolase
  • PTEN protein, human