ERF is a Potential ERK-Modulated Tumor Suppressor in Prostate Cancer

Abstract

Half of all prostate cancers contain an oncogenic gene fusion between the androgen-regulated upstream elements of the TMPRSS2-gene with the consequently upregulated ETS transcription factor ERG. Despite this high prevalence, detecting the presence of TMPRSS2-ERG in patients tumors has little-to-no useful clinical utility, in part due to a lack of understanding of its mechanisms of oncogenesis. I have characterized a gene, ERF, which functions as a putative tumor suppressor. I had hypothesized that ERF is outcompeted by the TMPRSS2-ERG gene product. Currently, I have identified how ERF and ERG may compete with each other, and as a result, have opposing effects on cancer cell proliferation. I am currently now investigating the tumor suppressor function of ERF in prostate cancers lacking TMPRSS2-ERG.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2017
Accession Number
AD1048741

Entities

People

  • Rohit Bose

Organizations

  • Sloan-Kettering Institute

Tags

DTIC Thesaurus Topics

  • Androgen Receptors
  • Androgens
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Gene Expression
  • Genetics
  • Health Services
  • Medical Personnel
  • Mrna
  • Neoplasms
  • Prostate
  • Prostate Cancer
  • Proteins
  • Statistical Analysis
  • Stem Cells
  • Transcription Factors

Readers

  • Logistics and Supply Chain Management.
  • Molecular and genetic basis of cancer.