C-erbB-2 expression and its relationship with ploidy, p53 abnormalities and epidermal growth factor receptor content in human non-small cell lung cancer

Clin Chim Acta. 1999 Jul;285(1-2):105-20. doi: 10.1016/s0009-8981(99)00113-8.

Abstract

This study attempts to clarify the role of c-erbB-2 overexpression in human non-small cell lung cancer (NSCLC) and relate it with the p53 alterations, DNA index (D.I.) and epidermal growth factor receptor (EGFR) content in sixty four patients with NSCLC. c-erbB-2 and EGFR quantification were carried out from tissue homogenates using quantitative ELISA procedures. p53 alterations were determined by immunohistochemical (IHC) detection with the monoclonal antibody DO-7 and analysis for p53 mutations on exons 4 to 8 by single strand conformation polymorphism (SSCP). The D.I. was performed by flow cytometry. c-erbB-2 hyperexpression was found in 13 of 58 LC (22%), and it was closely associated with hyperdiploid tumors (D.I. >1.3; P = 0.00). The p53 abnormalities detected by SSCP were statistically more frequent in hyperdiploid tumors (16/25; P = 0.015) than in diploid ones (8/30). No relationship between the results of IHC p53 and SSCP was found. The patients with c-erbB-2 hyperexpressing tumors were prone to have frequent relapses (P = 0.03), although the patients with hyperdiploid NSCLC are the ones with the highest relapse rate (P = 0.008). From the results obtained in this study the following conclusions can be drawn: (a) c-erbB-2 hyperexpressing NSCLC are associated with abnormalities in other biological markers and with a greater rate of relapses; (b) SSCP seemed to be more specific that IHC to detect p53 molecular abnormalities; and (c) the D.I. is the parameter more tightly related with relapse.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / metabolism*
  • ErbB Receptors / metabolism*
  • Humans
  • Immunohistochemistry
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Ploidies*
  • Receptor, ErbB-2 / genetics*
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • Tumor Suppressor Protein p53
  • ErbB Receptors
  • Receptor, ErbB-2