The purpose of this study is to determine whether quinacrine is effective in the treatment of Androgen-Independent Prostate Cancer.
Despite a modest improvement in survival with available chemotherapy treatments, androgen-independent metastatic prostate cancer remains essentially incurable. Several changes in gene function that characterize malignancy have been identified. For example the p53 gene in normal tissue lessens the risk of cancer through growth arrest or cell suicidal programs. Thus the silenced p53 gene present in cancer tissue contributes to the growth of the cancer. In addition when the p53 gene is silenced, a cell survival pathway, controlled by the NF-kB gene, is activated leading increased cell survival. Quinacrine can activate p53 and inhibit NF-kB, thus reestablishing cell suicidal programs and decreasing cell survival in cancer tissue. Moreover, quinacrine is effective against several prostate tumor cell lines in vitro, and has anti-tumor effects against prostate cancer xenografts in mice.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
31
100 mg daily
Efficacy of Quinacrine, Based on Prostate Specific Antigen (PSA) Response in Patients With Androgen-independent Metastatic Prostate Cancer
Patients who achieved a complete response (CR) or a partial response (PR) to therapy were allowed to continue to receive treatment until disease progression or unacceptable toxicity occurred, until the patient discontinued treatment for another reason, or for a total of 6 months. Patients who continued to show a CR or PR or who maintained stable disease (SD) after 6 months of therapy were to be allowed to continue therapy at the investigator's discretion.
Time frame: End of treatment
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