Journal
CLINICAL GENITOURINARY CANCER
Volume 5, Issue 7, Pages 457-459Publisher
CIG MEDIA GROUP, LP
DOI: 10.3816/CGC.2007.n.036
Keywords
androgen-deprivation therapy; myelodysplastic syndrome; prostate-specific antigen
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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 hypornethylating DNA that leads to the reversal of gene silencing. It is hypothesized that the addition of azaciticline 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.
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