A case of a 32-year-old patient who presented with vaginal bleeding 2 years after undergoing laparoscopic radical trachelectomy and vaginal cerclage was noted to have Mersilene tape erosion. Subsequent management includes the removal of displaced Mersilene tape and a repeat cerclage through a new technique of laparoscopic abdominal cerclage to avoid repeat tape erosion. The novel technique of laparoscopic abdominal cerclage to lower the incidence of preterm delivery among pregnant patients who underwent laparoscopic radical trachelectomy for early-stage cervical cancer is described.
To evaluate the clinical possibility of using a microlaparoscope in laparoscopically assisted vaginal hysterectomy.Twenty-five women with different indications for hysterectomy and a uterine size < 14 weeks' gestation underwent laparoscopically assisted vaginal hysterectomy using a microlaparoscope and 2-mm instruments.Microlaparoscopic procedures included coagulation and separation of infundibulopelvic or uteroovarian round ligaments, vesico-uterine-visceral peritoneal fold dissection, and anterior and posterior colpotomy. The mean operative time, blood loss and length of hospital stay were 84.40 +/- 16.85 minutes, 262.00 +/- 112.99 mL and 3.08 +/- 0.64 days, respectively. No patients developed serious complications, but there were two minor ones.Microlaparoscopy appears to be an efficacious alternative treatment option in well-selected patients undergoing laparoscopically assisted vaginal hysterectomy.
This study was conducted to describe the feasibility of treating endometrial cancer with hysterectomy, bilateral salpingo-oophorectomy, and bilateral pelvic lymphadenectomy by natural orifice transluminal endoscopic surgery (NOTES). Women with early-stage endometrial cancer underwent surgical staging by transvaginal NOTES in a tertiary referral medical center, and surgical outcomes were measured. Three patients with a mean age of 46.3 [standard deviation (SD) = 2.5] years and a body mass index of 27.7 (SD, 2.4) kg/m2 were selected. The average operative time was 249.3 (SD, 49.3) minutes. All patients had minimal blood loss during the operation (<50 mL) without intraoperative blood transfusion. All of them had a surgical staging of pT1aN0M0 and FIGO IA. No intraoperative or postoperative complications were noted. No cases were converted to traditional laparoscopy or laparotomy. NOTES is a minimally invasive surgery and leaves only invisible scars. Our preliminary results showed the safety and feasibility of transvaginal NOTES in staging surgery for early-stage endometrial cancer. However, it should be evaluated in more cases.
Ovarian preservation before abdominal irradiation may be recommended for young patients with various types of invasive cancer. The most common site for ovarian transposition is just below the iliac crest or posterolateral to the uterus. Here, we demonstrate laparoscopic ovariopexy with an automatic stapling device to transpose the ovaries to an uncommon site, i.e. lower anterolateral abdomen, in a patient with medulloblastoma prior to her receiving irradiation of the craniospinal axis. The anterolateral transposition of the ovary not only kept it away from the irradiated field but allowed it also to be shielded by the uterus. Thus, ovarian function could be well preserved.
More than 25% of patients diagnosed with endometrial carcinoma have an invasive primary cancer accompanied by metastases. Gonadotropin-releasing hormone (GnRH) plays an important role in reproduction. In mammals, expression of GnRH-II is higher than GnRH-I in reproductive tissues. Here, we examined the effect of a GnRH-II agonist on the motility of endometrial cancer cells and its mechanism of action in endometrial cancer therapy. Immunoblotting and immunohistochemistry (IHC) were used to determine the expression of the GnRH-I receptor protein in human endometrial cancer. The activity of MMP-2 in the conditioned medium was determined by gelatin zymography. Cell motility was assessed by invasion and migration assay. GnRH-I receptor si-RNA was applied to knockdown GnRH-I receptor. The GnRH-I receptor was expressed in the endometrial cancer cells. The GnRH-II agonist promoted cell motility in a dose-dependent manner. The GnRH-II agonist induced the phosphorylation of ERK1/2 and JNK, and the phosphorylation was abolished by ERK1/2 inhibitor (U0126) and the JNK inhibitor (SP600125). Cell motility promoted by GnRH-II agonist was suppressed in cells that were pretreated with U0126 and SP600125. Moreover, U0126 and SP600125 abolished the GnRH-II agonist-induced activation of MMP-2. The inhibition of MMP-2 with MMP-2 inhibitor (OA-Hy) suppressed the increase in cell motility in response to the GnRH-II agonist. Enhanced cell motility mediated by GnRH-II agonist was also suppressed by the knockdown of the endogenous GnRH-I receptor using siRNA. Our study indicates that GnRH-II agonist promoted cell motility of endometrial cancer cells through the GnRH-I receptor via the phosphorylation of ERK1/2 and JNK, and the subsequent, MAPK-dependent activation of MMP-2. Our findings represent a new concept regarding the mechanism of GnRH-II-induced cell motility in endometrial cancer cells and suggest the possibility of exploring GnRH-II as a potential therapeutic target for the treatment of human endometrial cancer.
Integrin-linked kinase (ILK) localizes to focal adhesions, and interacts with the cytoplasmic tail of β subunits of integrins and couples them to the actin cytoskeleton. ILK may act as a kinase and transmit the signals in a phosphatidylinositol 3-kinase-dependent manner, or can act as a scaffold protein to function through cell–matrix interactions, cell signaling, and cytoskeletal organization. Within this pivotal position, ILK mediates many important cellular processes, including survival, proliferation, differentiation, adhesion, migration, contractility, etc. Besides, ILK plays some role in the activation of endothelial progenitor cells and neovascularization, and may also enhance vascular endothelial growth factor expression. Increased ILK activity may promote epithelial-to-mesenchymal transition and induce a transformed, tumorigenic phenotype. Higher expression of ILK was frequently noted in human malignancies. ILK may also be important for mitotic-spindle assembly. Inhibition of ILK causes proliferative defects, induces cell-cycle arrest and apoptosis, and is embryonically lethal. New concepts of gene or cell-based therapy working on the up- or downregulation of ILK have emerged as a valid therapeutic approach for cancer treatment, and also a new hope for vasculogenesis in the ischemic area. The current review will discuss some known mechanisms, and the role of ILK in the modulation of tumorigenesis and reproduction, based on an extensive literature survey.
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