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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Sonpavde, G; Aparicio, A; Guttierez, I; Boehm, KA; Hutson, TE; Berry, WR; Asmar, L; von Hoff, DD

Published Date

  • December 2007

Published In

Volume / Issue

  • 5 / 7

Start / End Page

  • 457 - 459

PubMed ID

  • 18272030

Pubmed Central ID

  • 18272030

International Standard Serial Number (ISSN)

  • 1558-7673

Digital Object Identifier (DOI)

  • 10.3816/CGC.2007.n.036

Language

  • eng

Conference Location

  • United States