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Active cell death in hormone-dependent tissues

M P Tenniswood1, R S Guenette, J Lakins

  • 1Department of Biochemistry, Faculty of Medicine, University of Ottawa, Ontario, Canada.

Cancer Metastasis Reviews
|September 1, 1992
PubMed

Insights

Hormone ablation induces active cell death (ACD) in hormone-dependent tissues like the prostate. Differential sensitivity of epithelial cells to ACD is influenced by stromal interactions, impacting hormone resistance.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Oncology

Background:

  • Hormone-dependent tissues (prostate, mammary gland) undergo active cell death (ACD) upon hormonal manipulation.
  • ACD can be induced by hormone ablation, anti-hormones, calcium channel agonists, and TGF-beta.
  • Specific genes like TRPM-2, transglutaminase, PARP, and Hsp27 are upregulated during ACD.

Purpose of the Study:

  • To review the underlying biology of active cell death in prostate and mammary glands.
  • To discuss the relevance of ACD in the context of hormone resistance.
  • To explore the differential sensitivity of epithelial cells to ACD induction.

Main Methods:

  • Review of existing literature on active cell death in hormone-dependent tissues.
  • Analysis of gene expression changes associated with ACD.
  • Examination of cellular localization and stromal interactions in sensitive and resistant cell populations.

Main Results:

  • Hormone ablation and specific agents readily induce ACD in hormone-dependent epithelial cells.
  • Differential sensitivity to ACD exists among epithelial cells, influenced by location and stromal contact.
  • Prostatic secretory cells in distal ducts are sensitive; proximal cells are more resistant due to basal cell-stroma interaction.

Conclusions:

  • Stromal interactions play a critical role in modulating epithelial cell sensitivity to ACD.
  • Understanding ACD mechanisms is crucial for addressing hormone resistance in prostate and mammary gland cancers.
  • Further research into unidentified ACD-related genes may reveal new therapeutic targets.

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