Tumor hypoxia and expression of c-met in cervical cancer

Gynecol Oncol. 2007 Jan;104(1):181-5. doi: 10.1016/j.ygyno.2006.07.040. Epub 2006 Sep 22.

Abstract

Objectives: Hypoxia enhances malignant progression by promoting the development of metastases and increasing invasiveness. One key regulator that controls growth, invasion and metastasis in cancer cells is the growth factor receptor c-met. The aim of this study, therefore, was to investigate the expression of the c-met protooncogene in cervical cancers in relation to intratumoral hypoxia levels and to clinico-pathological parameters.

Methods: 43 Patients with cervical cancer were subjected to intratumoral pO(2) measurement with the Eppendorf electrode and biopsies were taken. The tissue was subsequently analyzed by immunohistochemistry with an anti-c-met antibody.

Results: c-met was expressed in 72% of cervical cancers. There was a significantly stronger expression in poorly differentiated tumors (r=0.4, p=0.008). Furthermore, c-met expression was significantly associated with a spray-like pattern of invasion (p=0.008). However, there was no significant relationship between c-met expression and intratumoral hypoxia, pT stage, FIGO stage, lymphovascular space involvement, tumor size or overall survival.

Conclusions: Although c-met has been shown to be hypoxia-induced in vitro, our results suggest that it is not the mediator of deleterious effects of hypoxia on clinical outcome in cervical cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Biopsy
  • Cell Hypoxia / physiology
  • Female
  • Humans
  • Middle Aged
  • Neoplasm Invasiveness
  • Oxygen / metabolism
  • Partial Pressure
  • Receptor Protein-Tyrosine Kinases / biosynthesis*
  • Uterine Cervical Neoplasms / enzymology*
  • Uterine Cervical Neoplasms / metabolism*
  • Uterine Cervical Neoplasms / pathology

Substances

  • RON protein
  • Receptor Protein-Tyrosine Kinases
  • Oxygen