Garrahan U-Stitch laparoscopic appendicovesicostomy - Making surgery easier.

Appendicovesicostomy is an established continent urinary conduit. The development of minimally invasive techniques and the reduction of operative time instigated the search for new techniques. In this video we show the laparoscopic transabdominal technique for appendicovesicostomy using U-stitch technique as proposed by Santiago Weller et al. We present a case of a teenager with neurogenic bladder and intolerance for urethral catheterization. The procedure was performed using a transperitoneal approach. The appendix was detached from the colon preserving its pedicle. The proximal appendix was spatulated and pulled through a hiatus created in the distal vesical mucosa into the bladder using a U-stitch, on a Shanfield fashion anastomosis in the anterior wall of the bladder. Detrusor was approximated over the appendix creating an antireflux mechanism. The tip of the appendix was brought out to the right iliac fossa and ostomy was fashioned. The operative time was 180 min. A Foley catheter was placed through the conduit. The case was done without any intraoperative or postoperative complications. Laparoscopic appendicovesicostomy with U-stitch technique is feasible and can be easily done in a short operative time in centers with expertise in laparoscopic surgeries with low complexity and high reproducibility.

C-kit and its ligand stem cell factor: potential contribution to prostate cancer bone metastasis.

The tyrosine kinase receptor c-kit and its ligand stem cell factor (SCF) have not been explored in prostate cancer (PC) bone metastasis. Herein, we found that three human PC cell lines and bone marrow stromal cells express a membrane-bound SCF isoform and release a soluble SCF. Bone marrow stromal cells revealed strong expression of c-kit, whereas PC cells showed very low levels of the receptor or did not express it all. Using an experimental model of PC bone metastasis, we found that intraosseous bone tumors formed by otherwise c-kit-negative PC3 cells strongly expressed c-kit, as demonstrated using immunohistochemical and Western blot analyses. Subcutaneous PC3 tumors were, however, c-kit-negative. Both bone and subcutaneous PC3 tumors were positive for SCF. Immunohistochemical analysis of human specimens revealed that the expression frequency of c-kit in epithelial cells was of 5% in benign prostatic hyperplasia, 14% in primary PC, and 40% in PC bone metastases, suggesting an overall trend of increased c-kit expression in clinical PC progression. Stem cell factor expression frequency was more than 80% in all the cases. Our data suggest that the bone microenvironment up-regulates c-kit expression on PC cells, favoring their intraosseous expansion.

Bone marrow stromal cells enhance prostate cancer cell invasion through type I collagen in an MMP-12 dependent manner.

At the cellular level, the process of bone metastasis involves many steps. Circulating cancer cells enter the marrow, proliferate, induce neovascularization, and ultimately expand into a clinically detectable, often symptomatic, metastatic deposit. Although the initial establishment and later expansion of the metastatic deposit in bone require tumor cells to possess invasive capability, the exact proteases responsible for this phenotype are not well known. The objective of our study was to take an unbiased approach to determine which proteases were expressed and functional during the initial interactions between prostate cancer cells and bone marrow stromal (BMS) cells. We found that the combination of human prostate cancer PC3 and BMS cells stimulates the invasive ability of cancer cells through type I collagen. The use of inhibitors for each of the major protease families indicated that 1 or more MMPs was/were responsible for the BMS-induced invasion. Gene profiling and semiquantitative RT-PCR analysis revealed an increased expression of several MMP genes because of PC3/BMS cell interaction. However, only MMP-12 showed an increase in protein expression. Downregulation of MMP-12 expression in PC3 cells by siRNA inhibited the enhanced invasion induced by PC3/BMS cell interaction. In vivo, MMP-12 was found to be primarily expressed by prostate cancer cells growing in bone. Our data suggest that BMS cells induce MMP-12 expression in prostate cancer cells, which results in invasive cells capable of degradation of type I collagen.