Evaluation of the epidermal growth factor receptor (EGFR) in colorectal tumours and lymph node metastases

J. A. McKay, L. J. Murray, Stephanie Curran, V. G. Ross, Caroline Clark, Graeme Ian Murray, J. Cassidy, H. L. McLeod

Research output: Contribution to journalArticle

178 Citations (Scopus)

Abstract

Overexpression of the epidermal growth factor receptor (EGFR) often correlates with an aggressive tumour phenotype and poor prognosis. To examine the relevance of EGFR in colorectal cancer, we determined the expression of EGFR protein in 249 colorectal adenocarcinomas and 42 lymph node metastases using immunohistochemistry. Moreover, we investigated a (CA)(n) dinucleotide repeat polymorphism of the EGFR gene in a subset of 114 tumours. High levels of EGFR protein were observed in 123/249 (49.4%) samples. EGFR expression in colorectal carcinomas correlated with differentiation grade (P = 0.014). However, there were no associations with Dukes' stage, site, patient age or gender. EGFR protein expression did not influence survival in this colorectal cancer patient cohort (P greater than or equal to 0.05). Expression was not identical in paired colorectal tumours and lymph node metastases, with only 17/42 (40.5%) samples showing equivalent EGFR levels (P > 0.05). The distribution of the (CA)(n) dinucleotide repeat alleles in colorectal adenocarcinomas was not associated with EGFR protein expression (P > 0.05). These results indicate that while EGFR overexpression is a common event in colorectal carcinogenesis, it does not influence patient prognosis. (C) 2002 Elsevier Science Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)2258-2264
Number of pages6
JournalEuropean Journal of Cancer
Volume38
Issue number17
DOIs
Publication statusPublished - Nov 2002

Keywords

  • colorectal cancer
  • epidermal growth factor receptor
  • prognosis
  • polymorphism
  • immunohistochemistry
  • lymph node metastases
  • colon carcinoma cells
  • dinonucleotide repeat
  • signaling network
  • nuclear antigen
  • cyclin D1
  • cancer
  • expression
  • overexpression
  • intron 1

Cite this