Expression of HIF-1alpha and iNOS in astrocytic gliomas: a clinicopathological study

In Vivo. 2006 May-Jun;20(3):421-5.

Abstract

Background: Hypoxia-inducible-factor-1 (HIF-1) is present at high levels in human tumors and plays a crucial role in tumor promotion by up-regulating several target genes. HIF-1 stimulates the production of NO through the induction of inducible NO synthase (iNOS).

Patients and methods: Sixty-three human astrocytic gliomas were analyzed by immunohistochemistry for HIF-1alpha and iNOS using formalin-fixed paraffin-embedded material. In 39 cases, the results of immunohistochemistry were correlated with the clinical outcomes.

Results: HIF-1alpha was detected only in astrocytic gliomas grades III and IV, both in the nucleus and in the cytoplasm. The iNOS expression was increased in astrocytic gliomas grades I, II and III and was statistically significantly decreased in astrocytic gliomas grade IV. iNOS was localized round the capillary vessels as well. Statistical analysis showed that the HIF-1alpha and iNOS expressions did not correlate with patient survival.

Conclusion: We believe that HIF-1alpha and iNOS expressions merit further investigations in order to understand the biology of astrocytic gliomas. More data are needed from prospective studies.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Astrocytoma / enzymology*
  • Astrocytoma / metabolism*
  • Astrocytoma / pathology
  • Biomarkers, Tumor / analysis*
  • Enzyme Induction
  • Female
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Nitric Oxide Synthase Type II / biosynthesis*
  • Nitric Oxide Synthase Type II / genetics
  • Retrospective Studies

Substances

  • Biomarkers, Tumor
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Nitric Oxide Synthase Type II