186 THE JOURNAL OF UROLOGY ® Vol. 179, No. 4, Supplement, Sunday, May 18, 2008 and other reasons (9 and 3 subjects, respectively). Seventeen ADT patients and 13 CS declined participation, resulting in inclusion of 20 ADT patients and 13 CS. ADT was given for 52 (0-141) months. In 3 of the 4 ADT patients newly diagnosed with DM2, the diagnosis was based on the two-hour glucose value. CONCLUSIONS: ADT is associated with a 20% prevalence of previously undiagnosed DM2, and the OGTT was usually required for diagnosis of DM2. Prospective studies need to determine if the relation between ADT and these metabolic changes is associative or causative, and if proper management of DM2 and MetS decreases the high risk for cardiovascular events in patients receiving ADT. Results Age (yrs) BMI (kg/ m 2 ) 2 hr glucose (mmol/L) Testosterone (nmol/L) DM2 (# of subjects) MetS (# of subjects) ADT (n=20) 75.4±10.7 27.4±2.1 7.4±3.3 2.14±6.03 4 (20%) 3 (15%) CS (n=13) 74.1±9.2 27.9±4.7 6.0±2.1 15.48±7.60 0 (0%) 4 (31%) Source of Funding: None 531 THE EFFECT OF ANDROGEN DEPRIVATION THERAPY ON THE RATE OF SUBSEQUENT NON-CANCER MORBIDITIES Nazareno Suardi*, Claudio Jeldres, Andrea Gallina, Shahrokh F Shariat, Alberto Briganti, Hugues Widmer, Andrea Salonia, Philippe Arjane, Markus Graefen, Fred Saad, Francesco Montorsi, Pierre I Karakiewicz. Milan, Italy, Montreal, QC, Canada, Dallas, TX, and Hamburg, Germany. INTRODUCTION AND OBJECTIVE: Androgen deprivation patients. This treatment modality exposure has been shown to be associated to a subsequent increase in the rate of other comorbidities. We examined the effect of ADT exposure time on the rate of 12 different comorbidities in a large administrative database. METHODS: The study population consisted of 28510 prostate cancer patients diagnosed between 1983 and 2004. Of these, 10787 (37.8%) were treated with androgen deprivation therapy according to medication codes. Exposure to more than 1.5 year was recorded in 6437 patients (59.7%). The addressed comorbidities consisted of: myocardial infarction, congestive heart failure, peripheral vascular disease, dementia, cerebro-vascular disease, chronic pulmonary disease, connective tissue disease, ulcer disease, moderate to severe renal disease, diabetes, mild liver disease and moderate to severe liver disease. Univariable and multivariable Cox regression analyses were performed. Covariates included age, anti-androgen therapy exposure and comorbidities acquired prior to the date of the diagnosis of the comorbidity of interest. Each comorbidity was addressed in a separate analysis and was excluded from the list of covariates. RESULTS: In univariable analyses, the rates of myocardial were elevated in ADT exposed patients relative to unexposed ones. In multivariable analyses, after adjusting for age and anti-androgen therapy exposure, virtually all rates of these morbidities were increased in ADT exposed individuals. After controlling for other comorbidities using the time-dependent covariates approach and coding other comorbidities as cubic splines, only the dementia (p=0.02) and chronic pulmonary disease (p=0.01) maintained their independent predictor status. CONCLUSIONS: Exposure to ADT is associated with an increased risk of developing dementia and chronic pulmonary disease. Lack of detailed control for the confounding effect of comorbidities and of variable ADT exposure time may falsely exaggerate the strength of the association between ADT and other morbidities. Source of Funding: None Prostate Cancer: Basic Research (III) Moderated Poster Session 18 Sunday, May 18, 2008 3:30 - 5:30 pm 532 TRANSCRIPTION FACTOR STAT5 SYNERGIZES WITH ANDROGEN RECEPTOR IN PROSTATE CANCER CELLS Zhiyong Liao*, Shyh-Han Tan, Ayush Dagvadorj, Feng Shen, Lei Gu, Junaid Abdulghani, Ying Zhang, Edward P Gelmann, Tobias Zellweger, Zoran Culig, Tapio Visakorpi, Lukas Bubendorf, Robert A Kirken, James Karras, Marja T Nevalainen. Philadelphia, PA, Washington, DC, Basel, Switzerland, Innsbruck, Austria, Tampere, Finland, El Paso, TX, and Carlsbad, CA. INTRODUCTION AND OBJECTIVE: The molecular mechanisms underlying progression of prostate cancer to the hormone- independent state are poorly understood. We have previously shown that signal Transducer and Activator of Transcription 5a/b (Stat5a/b) is critical for the viability of human prostate cancer cells. We have also shown that Stat5a/b is constitutively active in high grade human prostate cancer, but not in normal prostate epithelium. Furthermore, activation of Stat5a/b in primary human prostate cancer predicted early disease androgen-independent growth of prostate cancer. In this study, we prostate cancer cells. METHODS: Immunohistochemistry was performed to detect Transcriptional activity of AR and Stat5a/b in prostate cancer cells was levels were manipulated in prostate cancer cells by adenoviral gene delivery of a dominant-negative Stat5a/b (DNStat5a/b) mutant of Stat5a/b with wild-type Stat5a/b (WtStat5a/b) as a control. Physical interaction between Stat5a/b and AR was detected by immunoprecipitation and immunoblotting in prostate cancer cells. Electrophoretic mobility RESULTS: We demonstrate here that transcription factor Stat5a/b is active in 95% of clinical hormone-refractory human prostate Stat5a/b increases transcriptional activity of AR, and AR, in turn, increases transcriptional activity of Stat5a/b. Liganded AR and active Stat5a/b physically interact in prostate cancer cells and, importantly, because Stat5a/b and AR are both transcription factors that inhibit apoptosis and promote growth of prostate cancer cells. CONCLUSIONS: The work presented here provides the signaling protein Stat5a/b in human prostate cancer cells. Source of Funding: American Cancer Society grant RSG- 04-196-01-MGO, Department of Defense Prostate Cancer grant W81XWH-05-01-0062, and NIH NCI grant 1RO1CA113580-01A1. This project was funded, in part, under a grant with the Pennsylvania Department of Health. 533 MIR-125b INDUCES ANDROGEN-INDEPENDENT GROWTH OF PROSTATE CANCER CELLS Xu-Bao Shi*, Lingru Xue, Joy Yang, Christopher P Evans, Ralph W deVere White. Sacramento, CA. INTRODUCTION AND OBJECTIVE: Increasing evidence has shown that some aberrantly-expressed microRNAs (miRNAs) are involved in human carcinogenesis. Recently, we found that androgen- independent (AI) LNCaP sublines (cds cells) express markedly increased miR-125b compared to the parental LNCaP cells, suggesting that this miRNA may play a role in the pathogenesis of prostate cancer (CaP).