The molecular pathology of urological malignancies

J Pathol. 1997 Dec;183(4):380-7. doi: 10.1002/(SICI)1096-9896(199712)183:4<380::AID-PATH959>3.0.CO;2-7.


Urological malignancies kill over 16,000 people annually in England and Wales. There have been exciting recent developments in our understanding of the molecular pathogenesis of these diseases, although many questions remain unanswered. Three separate genes (WT1, WT2, and WT3) have been implicated in Wilms' tumour development. Patients with von Hippel-Lindau (VHL) syndrome develop renal cell carcinoma and it has been shown that VHL protein inhibits elongin, a cellular transcription factor which controls RNA elongation. Use of molecular markers to identify superficial bladder tumours likely to progress to muscle invasive disease has met with some success. Increased epidermal growth factor receptor (EGFR) and p53 expression, and decreased E-cadherin expression all correlate with tumour progression. Tumours in patients with carcinoma in situ have distinct molecular features. Androgen ablation delays disease progression in men with prostate cancer, but relapse is inevitable. Research has been directed towards elucidating the mechanisms by which prostate cancer 'escapes' hormonal control. Mutations in the androgen receptor have been identified. It is apparent that locally produced growth factors mediate androgen-dependent processes and these too have been implicated in prostate carcinogenesis.

Publication types

  • Review

MeSH terms

  • Carcinoma, Renal Cell / genetics
  • Humans
  • Kidney Neoplasms / genetics
  • Male
  • Prostatic Neoplasms / genetics
  • Urinary Bladder Neoplasms / genetics
  • Urogenital Neoplasms / genetics*
  • Wilms Tumor / genetics