Clinical evidence of distinct subgroups of astrocytic tumors defined by comparative genomic hybridization

Hum Pathol. 2000 May;31(5):608-14. doi: 10.1053/hp.2000.6686.

Abstract

In astrocytic tumors, the relationship between genetic pathways and patients' prognoses has not been fully investigated. In our studies of astrocytic tumors using comparative genomic hybridization, the presence of 8q gain was mutually exclusive of 7p gain or amplification. In this study, 45 cases of astrocytic tumor were divided into 3 groups: those with 7p gain, cases with 8q gain, or those with neither; and their clinical course, p53, and epidermal growth factor receptor (EGFR) expressions and proliferative activity were then compared. Of the cases examined, 17 (12 glioblastomas and 5 anaplastic astrocytomas) showed 7p gain. Eleven cases (5 glioblastomas, 2 anaplastic, and 4 low-grade astrocytomas) showed 8q gain. p53 accumulation was observed more frequently in cases with 8q gain than in those with 7p gain. Astrocytic tumors with 8q gain occurred more frequently in younger patients than those with 7p gain. Kaplan-Meier survival rate analysis showed higher survival rates in patients with 8q gain than in those with 7p gain. This tendency also was observed when only patients with malignant glioma were included in the survival analysis. Our results provide evidence for distinct clinical manifestations in astrocytic tumors with 8q and 7p gain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Astrocytoma / classification*
  • Astrocytoma / metabolism
  • Brain Neoplasms / classification*
  • Brain Neoplasms / metabolism
  • ErbB Receptors / metabolism
  • Female
  • Gene Amplification
  • Gene Dosage
  • Glioblastoma / classification*
  • Glioblastoma / metabolism
  • Humans
  • Immunohistochemistry
  • Ki-67 Antigen / metabolism
  • Male
  • Middle Aged
  • Nucleic Acid Hybridization
  • Polymorphism, Single-Stranded Conformational
  • Survival Analysis
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Ki-67 Antigen
  • Tumor Suppressor Protein p53
  • ErbB Receptors