Understanding and Targeting Cell Growth Networks in Breast Cancer

Abstract

In this second annual review, we have demonstrated that Arf-null MMECs contain unique polysome mRNA profiles, up-regulated Drosha levels, and a novel miRNA signature. We have also determined that significant crosstalk exists between the MAPK and mTOR pathways to ultimately regulate ARF mRNA translation in response to oncogenic RasV12 signals. We now understand the translational regulation of NPM. We have identified FBP1 as a key binding protein and repressor of the NPM 3?-UTR. We now have mouse models aimed at understanding the complex functional interactions between ARF, NPM, and DDX5. We have generated two double knockout mouse models that help to clarify the perceived interaction of these proteins. Loss of one allele of Npm1 or Ddx5 results in a partial rescue of Arf loss with regard to tumor incidence. Taken together, these insightful findings bring us significantly closer to our goal of understanding how signaling pathways impact major tumors suppressors in the control of cell growth

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Apr 01, 2010
Accession Number
ADA532380

Entities

People

  • Jason D Weber

Organizations

  • University of Washington

Tags

DTIC Thesaurus Topics

  • Antibodies
  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Carrier Proteins
  • Cells
  • Co-Channel Interference
  • Coding
  • Epithelial Cells
  • Genetics
  • Growth Factors
  • Mass Spectrometry
  • Neoplasms
  • Organelles
  • Proteins
  • Rna Stability
  • Spectrometry

Fields of Study

  • Biology

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular Biology and Genetics
  • Systems Analysis and Design