Targeting Nuclear FGF Receptor to Improve Chemotherapy Response in Triple-Negative Breast Cancer

Abstract

During this funding period, we determined an optimal window of time (8 days post chemotherapy-treatment) in which to study chemo-resistance signaling in chemo-residual triple-negative tumor cells, establishing an in vitro model of triple-negative breast cancer dormancy/recurrence. This work resulted in a manuscript publication. Using this model, we investigated the effect of reducing FGF receptor 2 expression in TN tumor cells on their chemo-resistance. This data showed that FGFR2 does not drive chemoresistance in this breast cancer sub-type, disproving our original hypothesis. Using a Novartis FGFR inhibitor, we confirmed a role for FGFR family members in TN tumor resistance, and obtained new data implicating FGF receptor 3 in this function. These data provide a foundation for testing FGFR3 regulation of TN tumor cell chemo-resistance in the next grant period.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2014
Accession Number
ADA612754

Entities

People

  • Robin E. Bachelder

Organizations

  • Duke University

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Chemotherapy
  • Combination Therapy
  • Culture Techniques
  • Inhibitors
  • Medical Personnel
  • Molecules
  • Neoplasms
  • Prostate Cancer
  • Proteins
  • Small Molecules
  • Therapy
  • Two Dimensional

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Materials Science.
  • Oncology