ERG alterations and mTOR pathway activation in primary prostate carcinomas developing castration-resistance

Pathol Res Pract. 2018 Oct;214(10):1675-1680. doi: 10.1016/j.prp.2018.08.031. Epub 2018 Aug 29.

Abstract

Introduction: One of the most common sites of distant metastasization of prostate cancer is bone, but to date reliable biomarkers able to predict the risk and timing of bone metastasization are still lacking.

Patients and methods: Surgically resected paraffin embedded samples from 12 primary prostate cancers that developed metachronous bone metastasis at different time points were studied (six cases within 2 years, six cases after 5 years from surgery). A targeted next-generation DNA and RNA sequencing able to assess simultaneously mutations, copy number alterations and fusion events of multiple genes was used. Immunohistochemistry was used to assess mTOR pathway activation.

Results: Rearrangements of ETS family genes, molecular alterations in PTEN and TP53 genes were detected in 10, 6 and 5 cancers, respectively. Nine samples showed TMPRSS2-ERG fusions, which were associated with increased ERG expression at immunohistochemistry. mTOR pathway activation was documented in 6 patients, with a clear trend of prevalence in late-metastatic patients (p = 0.08).

Conclusions: A simultaneous next-generation targeted DNA and RNA sequencing is applicable on routine formalin-fixed paraffin-embedded tissues to assess the multigene molecular asset of individual prostate cancers. This approach, coupled with immunohistochemistry for ERG and mTOR pathway proteins, may help to better characterize prostate cancer molecular features with a potential impact on clinical decisions.

Keywords: Bone metastasis; Castration resistance; Multigene panels; Next-generation sequencing; Prostate cancer.

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology*
  • Aged
  • Biomarkers, Tumor / genetics*
  • DNA Copy Number Variations / genetics
  • Humans
  • Male
  • Middle Aged
  • Mutation
  • Oncogene Proteins, Fusion / genetics
  • Prostatic Neoplasms, Castration-Resistant / genetics
  • Prostatic Neoplasms, Castration-Resistant / metabolism
  • Prostatic Neoplasms, Castration-Resistant / pathology*
  • Signal Transduction / physiology
  • TOR Serine-Threonine Kinases / genetics*
  • TOR Serine-Threonine Kinases / metabolism
  • Transcriptional Regulator ERG / genetics
  • Transcriptional Regulator ERG / metabolism

Substances

  • Biomarkers, Tumor
  • ERG protein, human
  • Oncogene Proteins, Fusion
  • Transcriptional Regulator ERG
  • MTOR protein, human
  • TOR Serine-Threonine Kinases