As of now, treatment of non-organ confined prostatic carcinoma requires either surgical or pharmacological castration. While surgery and radiation therapy are also effective for treatment of localized tumors, there is no effective cure for advanced or metastatic tumors, tumors made up of cancerous cells which migrate from the original site to other sites in the body. Hormonal therapies and chemotherapy are also available but they are generally ineffective in dealing with the advanced stages of prostate cancer. (Kondo, et al., 2000). The aim of therapy is to prevent androgenic stimulation of the tumor. Efforts to remove the tumor and the surrounding tissue with androgen ablation are often combined with the blockade of the androgen receptor by various anti-androgens. Androgens are responsible for the regulation of growth

Another experimental form of treatment for prostate cancer involves the construction of a novel chain fusion receptor named Pz-1 specific for the prostate-specific membrane antigen (PSMA). PSMA is a cell-surface glycoprotein expressed on prostate cancer cells and its expression is increased in the later stages of advanced prostate cancer, which include metastatic cells as well as hormone-deprived cells (Gong, et al., 1999). Gene transfer efficiency was monitored by fluorescence-activated cell sorter and gene take up by the T cells varied between 20% and 50% in a cultured medium. Results show that upon contact, these T cells readily lyse prostate cancer cells. The modified T cells also effectively targeted, PC-3, a human prostate cancer cell line normally negative for PSMA, when transduced with a retrovirus encoding PSMA. These findings suggest that adoptive cell therapy, using genetically engineered T cells in prostate cancer patients, can be an effective approach in treating prostate cancer (Gong, et al., 1999).

PC-3 cells transplanted subcutaneously in mice were given daily injections of 2-5A-anti-hTR in the presence of Lipofectamine when the tumors reached 50mm3 in volume (Kondo, et al., 2000). The optimal ratio of 2-5A-anti-hTR to Lipofectamine seemed to be 1 nmol of 2-5A-anti-hTR to 0.3 ìl Lipofectamine. After the series of treatments for 7 days, the increase in PC-3 tumor volume was just 14% when compared to the 215% tumor volume increase in the control group. The cell viability of tumors was reduced

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America Kondo, PSMA PSMA, PSMA-specific J591, Developing PSMA-specific, prostate cancer, et al, Fan Prostate, cancer cells, prostate cancer cells, GDEPT OAdV220, et al 2000, voeks et al, gong et al, et al 1999, gong et, al 1999, voeks et, al 2000, al 2002, kondo et, fludarabine phosphate,