ERG rearrangement in local recurrences compared to distant metastases of castration-resistant prostate cancer

Virchows Arch. 2012 Aug;461(2):157-62. doi: 10.1007/s00428-012-1270-7. Epub 2012 Jul 6.

Abstract

Castration-resistant prostate cancer is the second most common cause of cancer death and results in a median survival of less than 2 years. In prostate cancer, fusions between TMPRSS2 and ERG are common. The ERG rearrangement prevalence in local recurrent castration-resistant prostate cancer compared to distant metastatic prostate cancer is unknown. We investigated the frequency of ERG rearrangement in local recurrent castration-resistant prostate cancer compared to distant metastatic prostate cancer, and assessed for associations between androgen receptor (AR) amplification and ERG rearrangement status. Samples from 134 patients diagnosed with prostate cancer (84 local recurrent castration resistant prostate cancer, 55 distant metastatic prostate cancer) were assessed for their ERG rearrangement and AR amplification status by fluorescence in situ hybridization. Statistical analysis was performed using the χ (2) test. We found that the ERG rearrangement occurs at a significantly lower frequency in distant metastatic prostate cancer (25 %) than in local recurrent castration-resistant prostate cancer (45 %). The AR amplification frequencies were 45 and 35 % in local recurrent castration-resistant prostate cancer and distant metastatic prostate cancer, respectively. The ERG rearrangement occurred at a lower frequency in distant metastatic prostate cancer compared to local recurrent castration-resistant prostate cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Hormonal / therapeutic use
  • Castration / methods
  • Drug Resistance, Neoplasm / genetics*
  • Gene Amplification
  • Gene Rearrangement*
  • Humans
  • In Situ Hybridization, Fluorescence
  • Male
  • Neoplasm Metastasis
  • Neoplasm Recurrence, Local / genetics
  • Neoplasm Recurrence, Local / pathology
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology*
  • Receptors, Androgen / genetics
  • Tissue Array Analysis
  • Trans-Activators / genetics*
  • Transcriptional Regulator ERG

Substances

  • Antineoplastic Agents, Hormonal
  • ERG protein, human
  • Receptors, Androgen
  • Trans-Activators
  • Transcriptional Regulator ERG