Breast Cancer Chemoresistance Mechanisms Through PI 3-Kinase and Akt Signaling

Abstract

We have discovered that the Akt pathway modulates breast cancer cell survival in response to genotoxic agents, and discovered a new substrate of Akt,MERIT40, that is phosphorylated upon exposure of cells to chemotherapeutic drugs. We propose that this represents a major mechanism by which cells exposed to these drugs evade cell death by apoptosis and thus become resistant to the damaging effects of clinically-relevant chemotherapy agents. These findings have important ramifications for the use of chemotherapy drugs in breast cancer patients, and many also suggest that MERIT40 may be used as a clinically relevant biomarker for resistance to doxorubicin.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2015
Accession Number
AD1007364

Entities

People

  • Alex Toker
  • Kristin Brown

Organizations

  • Beth Israel Deaconess Medical Center

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biological Markers
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Chemotherapy
  • Combination Therapy
  • Diseases And Disorders
  • Growth Factors
  • Medical Personnel
  • Neoplasms
  • Ovarian Cancer
  • Proteins
  • Therapy

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Prostate Cancer Biology.