Phase II study of azacitidine to restore responsiveness of prostate cancer to hormonal therapy

Guru Sonpavde, Ana Aparicio, Israel Guttierez, Kristi A. Boehm, Thomas E. Hutson, William R. Berry, Lina Asmar, Daniel D. Von Hoff

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Epigenetic alterations, including methylation of key tumor suppressor genes, may play a role in the progression of prostate cancer to a castration-refractory state. Azacitidine, an agent approved for the treatment of myelodysplastic syndromes, appears to exert its antineoplastic effects partly by hypomethylating DNA that leads to the reversal of gene silencing. It is hypothesized that the addition of azacitidine to complete androgen blockade may restore the responsiveness of progressive prostate cancer to hormonal therapy. A phase II trial was designed to evaluate the activity of azacitidine to primarily modulate PSA kinetics, with supportive secondary clinical endpoints. Correlative studies will be performed to detect the biologic activity of azacitidine (increased fetal hemoglobin, plasma DNA methylation) and examine any association with anti-tumor clinical activity.

Original languageEnglish (US)
Pages (from-to)457-459
Number of pages3
JournalClinical Genitourinary Cancer
Volume5
Issue number7
DOIs
StatePublished - Dec 2007

Keywords

  • Androgen-deprivation therapy
  • Myelodysplastic syndrome
  • Prostate-specific antigen

ASJC Scopus subject areas

  • Oncology
  • Urology

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