p53 and HER-2 alterations in renal cell carcinoma

Urology. 1997 Oct;50(4):636-42. doi: 10.1016/S0090-4295(97)00258-6.


Objectives: To investigate protein expression and genetic aberrations of p53 and HER-2 in renal cell carcinoma (RCC) as well as possible association of p53 and HER-2 abnormalities with the tumor behavior of RCC.

Methods: Formalin-fixed and paraffin-embedded tissue blocks from 70 patients with RCC were studied. Protein expression of p53 and HER-2 was assessed immunohistochemically. Following deoxyribonucleic acid extraction from the paraffin sections using a microdissection technique, p53 gene mutations within exons 5 to 8 were examined by polymerase chain reaction (PCR) single-strand conformation polymorphism and HER-2 gene amplification by a differential PCR.

Results: Of the 70 RCCs, 16 (22.9%) showed protein expression of p53, with 7 (10%) demonstrating mutations within exons 5 to 7. Additionally, 28 RCCs (40%) displayed protein expression of HER-2, with 12 (17.1%) demonstrating gene amplification. All cases showing p53 mutations or HER-2 amplification represented protein expression of p53 or HER-2, respectively. No cases with negative immunostaining for p53 or HER-2 protein displayed positive results at gene level. Statistical analysis revealed a close relationship between p53 protein expression and the tumor grade, as well as a significant association of HER-2 protein expression and gene amplification with the tumor stage of RCC.

Conclusions: Our observations suggest that the abnormalities of p53 and HER-2 may be involved in the pathogenesis of RCC and that other mechanisms leading to protein expression of p53 and HER-2 may coexist within a single tumor in addition to the genetic aberrations.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Carcinoma, Renal Cell / genetics*
  • Carcinoma, Renal Cell / metabolism
  • Female
  • Genes, erbB-2 / genetics*
  • Genes, p53 / genetics*
  • Humans
  • Kidney Neoplasms / genetics*
  • Kidney Neoplasms / metabolism
  • Male
  • Middle Aged
  • Mutation
  • Oncogene Proteins v-erbB / biosynthesis
  • Tumor Suppressor Protein p53 / biosynthesis


  • Oncogene Proteins v-erbB
  • Tumor Suppressor Protein p53