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 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.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2018
Accession Number
AD1093079

Entities

People

  • Rohit Bose

Organizations

  • Sloan-Kettering Institute

Tags

DTIC Thesaurus Topics

  • Androgens
  • Biomedical Research
  • Cancer
  • Diseases And Disorders
  • Gene Expression
  • Genes
  • Genetics
  • Molecules
  • Mrna
  • Neoplasms
  • New York
  • Prostate
  • Prostate Cancer
  • Proteins
  • Suppressors
  • Transcription Factors
  • Transcriptomics

Readers

  • Molecular and genetic basis of cancer.
  • Oncology (Cancer Research).