Patients and Methods: The records of 2000 men who underwent RALP from February 2006 to April 2010 were retrospectively reviewed. A total of 80 men had undergone TURP

before RALP. A match-paired analysis was performed using our database to identify 80 additional men without a history of TURP with equivalent clinicopathologic selleckchem characteristics to serve as a control group (non-TURP group). The parameters compared included patient preoperative clinicopathologic characteristics, intraopeoperative characteristics, postoperative oncologic characteristics, minor and major postoperative complications, continence, and potency.

Results: The mean time between TURP and RALP was 3.6 months (3-6 months). Regarding preoperative characteristics, a statistical difference was only observed regarding preoperative patient potency in the TURP vs non-TURP group. Regarding intraopeoperative characteristics,

a statistical difference was observed regarding the need for bladder neck reconstruction and skin-to-skin operative time. Regarding postoperative pathologic characteristics, the positive surgical margin rate was not significant when the two groups were compared. The continence and potency rates in 12 months were similar (87.5%/91.25%) and (70.3%/86.5%) for both patient cohorts.

Conclusion: Although the procedure is technically more demanding, exhibits a prolonged operative time and time interval before continence and potency returns, it can be safely performed without compromising functional results as well as the radical nature of cancer surgery.”
“The Cyclopamine chemical structure chromosomal 5-Fluoracil translocation t(8;21) often found in acute

myeloid leukemia generates an oncogenic fusion protein AML1-ETO. This chimeric oncoprotein disrupts wild-type AML1 function and dysregulates genes important for normal myelopoiesis. Monoclonal antibodies that can capture and detect the AML1-ETO fusion protein would help with early diagnosis and treatment prognosis of acute myeloid leukemia. We report the development of murine monoclonal antibodies (MAbs) that specifically bind epitopes encoded by either AML1 or ETO. Since alignment to the human ETO protein indicated almost 100% homology to the mouse ortholog, a strategy was needed to instruct humoral immunity in mice to focus and respond to self-epitopes. Our strategy to develop capture/detector reagents involved producing MAbs that would bind to epitopes within the non-fused myelopic protein (i.e., either AML1 or ETO). This included a process to select antibodies for their ability to also recognize the translocated chromosomal AML1-ETO fusion protein and to identify complementary capture/detector antibody pairs. Construction of a peptide hapten-carrier complex and use of a rapid immunization protocol resulted in IgM-IgG ETO specific MAbs.