EGF-r gene copy number changes in renal cell carcinoma detected by fluorescence in situ hybridization

J Pathol. 1998 Apr;184(4):424-9. doi: 10.1002/(SICI)1096-9896(199804)184:4<424::AID-PATH1223>3.0.CO;2-A.

Abstract

Expression of epidermal growth factor receptor (EGF-r) is a frequent event in renal cell carcinoma (RCC). To investigate the role of EGF-r gene copy number changes related to EGF-r overexpression, 50 RCC specimens were examined by fluorescence in situ hybridization (FISH) and immunohistochemistry. Dual-labelling FISH with a repetitive pericentromeric probe for chromosome 7 and a probe for the EGF-r gene (at 7p13) was performed to analyse the EGF-r copy number in relation to chromosome 7 copy number on a cell-by-cell basis. Polysomy 7 was frequent in all histological types of RCC. Chromosome 7 polysomy was found in 26 of 35 clear cell (74 per cent), nine of nine papillary, and three of three chromophobe RCCs. EGF-r gene copy number was closely associated with the chromosome 7 copy number on a cell-by-cell basis. No EGF-r gene amplifications were found. EGF-r positivity was found in 37 of 50 cases (74 per cent) by immunohistochemistry. EGF-r positivity was more common in clear cell (81 per cent) than in papillary tumours (40 per cent; P = 0.029). Neither chromosome 7 nor EGF-r gene copy number was associated with EGF-r expression, indicating that an increased gene dosage is not a mechanism of EGF-r overexpression in RCC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Renal Cell / genetics*
  • Carcinoma, Renal Cell / metabolism
  • Carcinoma, Renal Cell / pathology
  • Chromosomes, Human, Pair 7
  • ErbB Receptors / genetics*
  • ErbB Receptors / metabolism
  • Gene Dosage*
  • Gene Expression
  • Humans
  • In Situ Hybridization, Fluorescence
  • Ki-67 Antigen / metabolism
  • Kidney Neoplasms / genetics*
  • Kidney Neoplasms / metabolism
  • Kidney Neoplasms / pathology
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism

Substances

  • Ki-67 Antigen
  • Neoplasm Proteins
  • ErbB Receptors