Reactivation of Breast Cancer Micrometastases by Senescent Bone Marrow Stroma

Abstract

We developed an injury model to bone marrow stroma cultured in vitro from bone marrow samples from mice and human donors. We demonstrated that oxidative injury with H2O2 induces a reproducible time- and dose-dependent secretory senescence profile that consists of export of interleukin 6 (IL-6) by murine and human stroma and IL-8 by murine stroma and activation of TGF beta signaling. Using oxidative injury as a positive control, we demonstrated that estrogen deprivation induces secretory senescence in bone marrow stroma both in female mice and a premenopausal human female volunteer and activation of TGF beta signaling in mice. We defined the parameters for estrogen-induced secretory senescence in mouse and human marrow. Preliminary observations suggest that human marrow is more sensitive to estrogen deprivation-induced secretory senescence resulting in a greater and more sustained response. These data will be expanded to define the relationship between post menopausal status and secretory senescence and the effect on this stromal response on the capacity to support micrometastatic breast cancer cell dormancy.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2010
Accession Number
ADA542221

Entities

People

  • Robert Wieder

Organizations

  • University of Medicine and Dentistry of New Jersey

Tags

DTIC Thesaurus Topics

  • Biological Aging
  • Bone Marrow
  • Bones
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Culture Media
  • Data Analysis
  • Deprivation
  • Diseases And Disorders
  • Estrogens
  • Indicator Dyes
  • Medical Personnel
  • Neoplasms
  • Stromal Cells
  • Tumor Cell Line
  • Volunteers

Readers

  • Oncology (Cancer Research).