Objective: Prostate stem cell antigen is overexpressed in human transitional cell carcinoma.Materials and Methods: This is a systematic review article that involved 35 articles about Prostate Stem Cell Antigen Is Overexpressed in Human Transitional Cell Carcinoma (from indexes medicos) of 1985 until 2008 and search of many related topics.Results: However, despite these efforts, 50% of superficial tumors will continue to recur and as many as 30% will progress to muscle-invasive disease. Although radical cystectomy can salvage many patients with muscle-invasive cancers, a significant number go on to die from metastatic disease, for which there is currently no effective treatment. These data underscore the urgent necessity for better diagnostic and treatment strategies for superficial and invasive bladder cancers. Given the sensitivity of bladder cancer to BCG immunotherapy, there is a particular need to identify bladder cancer antigens for cellular and monoclonal antibodybased targeted immunotherapies. EGFR, for example, is overexpressed by a significant percentage of muscleinvasive bladder cancers. A recent study demonstrated that monoclonal antibody directed against EGFR slowed growth of a human transitional cell cancer in an orthotopic mouse model. Similarly, new bladder cancer markers have been identified that not only demonstrate high specificity for TCC but that also shows early promise as a clinical tool.Conclusion: One such marker, uroplakin II, is an urothelium-specific differentiation antigen that is expressed by; 40% of TCCs. Detection of uroplakin-positive cells in human sera has been associated with metastatic spread of bladder cancer cells and may identify patients with micrometastatic spread prior to undergoing cystectomy. PSCA is a glycosylphosphatidylinositol (GPI) anchored 123- amino-acid glycoprotein related to the Ly-6/Thy-1 family of cell surface antigens. PSCA expression in normal tissues is largely prostate specific, but we recently reported finding PSCA transcripts and protein in transitional epithelium of the bladder and neuroendocrine cells of the stomach. In situ hybridization and IHC analyses demonstrated PSCA expression in more than 80% of local and 100% of bone-metastatic prostate cancer specimens. Importantly, the intensity of PSCA expression increased with tumor grade and stage, which suggests its potential as an immunotherapeutic target for highrisk and metastatic prostate cancer. Supporting this hypothesis, we recently demonstrated that monoclonal antibodies against PSCA can inhibit tumor growth and metastasis formation and can prolong survival in mice bearing human prostate cancer xenografts. Also, Dannull et al. recently reported that a PSCA-derived peptide could elicit a PSCA-specific T-cell response in a patient with metastatic prostate cancer. Because PSCA is present at low levels in normal bladder, we asked whether PSCA is expressed in TCC. We also determined whether PSCA is overexpressed in bladder cancer compared with normal bladder and whether the level of expression correlates with bladder cancer stage or grade. We demonstrate that PSCA is expressed by amajority of both muscle- invasive and superficial tumors. Moreover, PSCA is overexpressed in virtually all nonmuscle invasive bladder tumors and in .30% of invasive and metastatic cancers. As with prostate cancer, expression increases with increasing tumor grade. Interestingly, the overexpression of PSCA that we observed in TCC is quantitatively more than that seen in prostate cancer with respect to tumor stage. These results support PSCA as a potential diagnostic and/or therapeutic target in bladder cancer.