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Pten inactivation and the emergence of androgen-independent prostate cancer

Michael M Shen1, Cory Abate-Shen

  • 1Center for Advanced Biotechnology and Medicine, and Department of Pediatrics, Cancer Institute of New Jersey, University of Medicine and Dentistry, New Jersey/RWJMS, 679 Hoes Lane, Piscataway, NJ 08854, USA. mshen@cabm.rutgers.edu

Cancer Research
|July 20, 2007
PubMed

Insights

Hormone refractory prostate cancer involves signaling pathways like phosphoinositide-3 kinase/Akt and Erk. These pathways in prostate epithelium may counteract androgen receptor signaling, impacting hormone independence.

Area of Science:

  • Oncology
  • Molecular Biology
  • Urology

Background:

  • Hormone refractory disease is a late-stage, lethal event in prostate cancer.
  • Understanding the mechanisms of hormone independence is crucial for treatment development.

Purpose of the Study:

  • To investigate the signaling pathways involved in the onset of hormone independence in prostate cancer.
  • To explore the role of epithelial-stromal interactions in androgen independence.

Main Methods:

  • Analysis of mouse models of prostate tumorigenesis.
  • Examination of phosphoinositide-3 kinase/Akt and Erk mitogen-activated protein kinase signaling pathways.
  • Investigation of androgen receptor signaling in prostate stroma.

Main Results:

  • The onset of hormone independence can be separated from disease progression.
  • Activation of phosphoinositide-3 kinase/Akt and Erk pathways in prostate epithelium is associated with hormone independence.
  • These epithelial pathways may counterbalance androgen receptor signaling in the stroma.

Conclusions:

  • Epithelial-stromal interactions play a significant role in the development of androgen independence.
  • Findings suggest potential therapeutic targets for hormone refractory prostate cancer.

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