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.

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Document Details

Document Type
Technical Report
Publication Date
Apr 01, 2021
Accession Number
AD1156470

Entities

People

  • Rohit Bose

Organizations

  • University of California, San Francisco

Tags

DTIC Thesaurus Topics

  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Computational Biology
  • Computational Science
  • Gene Expression
  • Genetic Structures
  • Genetics
  • Health Services
  • Information Science
  • Neoplasms
  • Peptide Growth Factors
  • Regression Analysis
  • Statistical Analysis
  • Stem Cells
  • Therapy

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