Hee Joon Kang

How to do single-port laparoscopic cholecystectomy using LEAN BACK technique

Single-port laparoscopic cholecystectomy has been proposed as a minimally invasive surgery with the advantages of better cosmesis and less pain. However, the complicated arrangement of the instruments can cause collisions and makes it difficult to perform cholecystectomy even by senior surgeons. Therefore, we propose a new retraction technique called ‘LEAN BACK technique’, which enables performance to improve the dissection of Calot’s triangle without collision as described (Video S1). Single port is introduced at the abdomen after 20 mm of incision has been carried out under the direct visual control at umbilicus. A 10-mm camera is gently advanced into the abdominal cavity and the gall bladder (GB) is retracted by grasper instrument for inspection of the GB and its infundibulum. By means of close vision of laparoscope, first suture can be performed over the parietal peritoneum of the diaphragm (Fig. 1a). Because the suture is not included in the diaphragm, any bleeding or damage on the diaphragm can be avoided. The end of the thread is clipped to prevent the loosening of the first suture site. The second suture is performed at the fundus of the GB. If the GB is long, suture can be done at the middle of corpus (Fig. 1b). The tension of the thread can be controlled by exposure of the infundibulum (Fig. 1c). Thread is fixed by the clip and the view of Calot’s triangle is achieved as the view that would have been made by grasper instrument (Fig. 1d). One articulating grasp instrument retracts the GB; one hook cautery progressively dissects the Calot’s triangle. This allows for common and standard dissection of the GB. After the cystic duct and arteries are dissected and skeletonized by articulating dissector instrument, they are clipped and then divided. Once cystic duct and artery have been freed, fibrous adhesion between the GB and the liver is taken down by the hook cautery. Finally, the GB is freed from its bed.

P2-15-11: Outcomes of Corrective Procedure with Vicryl Mesh as an Oncoplastic Surgery of the Breast.

Background: Both cosmetic and oncologic outcomes are becoming more important for breast cancer patients. Breast-conserving surgery (BCS) has an acceptable cosmetic result compared with mastectomy, but BCS is also associated with cosmetic failure. In this study, we evaluated the cosmetic outcome of reconstructive surgery with the absorbable implant vicryl mesh after BCS compared with the outcome of BCS alone. Methods: From May 2007 to December 2009, 101 patients were involved in this study at Hallym University Sacred Heart Hospital. We used absorbable implants made of folding vicryl mesh and wrapped them with Interceed. In 79 cases, BCS with vicryl mesh implantation was performed; in the other 56 cases, only BCS was performed. Patient satisfaction with cosmetic outcomes was evaluated. We also analyzed other factors that affected cosmetic outcomes, including patient ages, body mass indices, tumor locations, and removed breast tissue. Results: In the vicryl mesh implantation group, 65 of 79 patients (82.3%) were satisfied; in the BCS-only group, 24 of 56 patients (43%) were satisfied ( P P Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-15-11.

Abstract 1003: The inhibitory role of quercetin-induced Dickkopf-1 on the growth of 4T1 breast cancer cell line

Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL Introduction: The highly conserved Wnt/β-catenin canonical signaling pathway plays a crucial role in the normal development and tumor development. Although β-catenin is stabilized in about 50% of breast cancer, mutations in the Wnt/β-catenin signaling pathway are relatively rare. Dickkopf-1 (Dkk-1) was first identified as a secreted inhibitor of the canonical Wnt/β-catenin signaling pathway and increased Dkk-1 results in the inhibition of β-catenin dependent target gene expression. In this study, we investigated the effect of quercetin, a flavonoid, to regulate 4T1 breast cancer cells by inducing the expression of Dkk-1. Methods: Using a MTT assay, the inhibition of cell proliferation by quercetin (0-40μM) on 4T1 cancer cells was measured. Effects of quercetin (20μM) on Dkk-1 mRNA expression were detected by quantitative real-time RT-PCR. To test the regulation of Wnt/β-catenin signaling activity, 4T1 cells were transiently transfected with β-catenin repoter gene (Topflash). After treatment of quercetin(20μM) for 48 hours, transcriptional activity of β-catenin was estimated by luciferase assay. The protein stability of β-catenin was analyzed by Western blotting. To confirm the inhibitory effect of Dkk-1, MTT assay was performed after treatment of human-recombinant Dkk-1 (h-r-Dkk-1) on 4T1 cells. Results: The growth of 4T1 cells, treated with the indicated amount of quercetin (0-40μM) for 48 hours, were reduced in a dose-dependent manner (p=0.0002). Real-time RT-PCR revealed that the expression of Dkk-1 mRNA was significantly increased by about five-fold at 20μM of quercetin. Within 48 hours of treatment, a 20μM concentration of quercetin reduced β-catenin transcriptional activity by approximately 2-fold (p=0.0037). Protein stability of β-catenin was down-regulated by quercetin (20μM) in a time-dependent manner. Also the addition of h-r-Dkk-1 to 4T1 cell line showed a similar role in the inhibition of cell proliferation (p=0.0320). Conclusion: The present study investigated the possible existence of autocrine Wnt/β-catenin signaling for regulating breast cancer cell growth. quercetin showed a potent inhibitory role in the Wnt/β-catenin signaling activity as well as the growth of 4T1 breast cancer cells. Moreover, Dkk-1, as a negative regulator for Wnt/β-catenin signaling, was confirmed to be induced by quercetin. Therefore the present study suggest that Wnt/β-catenin signaling may be a promising target pathway for innovative treatment strategies of breast cancer. Aknowledgement : This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010-000-1266). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1003. doi:10.1158/1538-7445.AM2011-1003